Uploaded byveneethmathew
PPT, PDF13,399 views

Ch 16: The Molecular Basis of Inheritance

DNA is the genetic material that is faithfully replicated and passed from parents to offspring. James Watson and Francis Crick discovered the double helix structure of DNA in 1953, which explained how DNA could store and replicate the instructions for making organisms. Their model showed that DNA consists of two strands coiled around each other, with nucleotides on the strands bonded together through base pairing with adenine bonding only to thymine and guanine only to cytosine. This allows each strand to serve as a template for duplicating the other, explaining DNA's role in inheritance and allowing organisms to pass genetic information between generations.

Embed presentation

Downloaded 387 times
1 / 109
2 / 109
3 / 109
4 / 109
5 / 109
6 / 109
7 / 109
8 / 109
9 / 109
10 / 109
11 / 109
12 / 109
13 / 109
14 / 109
15 / 109
16 / 109
17 / 109
18 / 109
19 / 109
20 / 109
21 / 109
22 / 109
23 / 109
24 / 109
25 / 109
26 / 109
27 / 109
28 / 109
29 / 109
30 / 109
31 / 109
32 / 109
33 / 109
34 / 109
35 / 109
36 / 109
37 / 109
38 / 109
39 / 109
40 / 109
41 / 109
42 / 109
43 / 109
44 / 109
45 / 109
46 / 109
47 / 109
48 / 109
49 / 109
50 / 109
51 / 109
Most read
52 / 109
53 / 109
54 / 109
55 / 109
56 / 109
57 / 109
58 / 109
59 / 109
60 / 109
61 / 109
62 / 109
63 / 109
64 / 109
65 / 109
66 / 109
67 / 109
68 / 109
69 / 109
70 / 109
71 / 109
72 / 109
73 / 109
74 / 109
75 / 109
76 / 109
77 / 109
Most read
78 / 109
79 / 109
80 / 109
Most read
81 / 109
82 / 109
83 / 109
84 / 109
85 / 109
86 / 109
87 / 109
88 / 109
89 / 109
90 / 109
91 / 109
92 / 109
93 / 109
94 / 109
95 / 109
96 / 109
97 / 109
98 / 109
99 / 109
100 / 109
101 / 109
102 / 109
103 / 109
104 / 109
105 / 109
106 / 109
107 / 109
108 / 109
109 / 109
LECTURE PRESENTATIONS For CAMPBELL BIOLOGY, NINTH EDITION Jane B. Reece, Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson © 2011 Pearson Education, Inc. Lectures by Erin Barley Kathleen Fitzpatrick The Molecular Basis of Inheritance Chapter 16
Overview: Life’s Operating Instructions • In 1953, James Watson and Francis Crick introduced an elegant double-helical model for the structure of deoxyribonucleic acid, or DNA • DNA, the substance of inheritance, is the most celebrated molecule of our time • Hereditary information is encoded in DNA and reproduced in all cells of the body • This DNA program directs the development of biochemical, anatomical, physiological, and (to some extent) behavioral traits © 2011 Pearson Education, Inc.
Figure 16.1
Concept 16.1: DNA is the genetic material • Early in the 20th century, the identification of the molecules of inheritance loomed as a major challenge to biologists © 2011 Pearson Education, Inc.
The Search for the Genetic Material: Scientific Inquiry • When T. H. Morgan’s group showed that genes are located on chromosomes, the two components of chromosomes—DNA and protein—became candidates for the genetic material • The key factor in determining the genetic material was choosing appropriate experimental organisms • The role of DNA in heredity was first discovered by studying bacteria and the viruses that infect them © 2011 Pearson Education, Inc.
Evidence That DNA Can Transform Bacteria • The discovery of the genetic role of DNA began with research by Frederick Griffith in 1928 • Griffith worked with two strains of a bacterium, one pathogenic and one harmless © 2011 Pearson Education, Inc.
• When he mixed heat-killed remains of the pathogenic strain with living cells of the harmless strain, some living cells became pathogenic • He called this phenomenon transformation, now defined as a change in genotype and phenotype due to assimilation of foreign DNA © 2011 Pearson Education, Inc.
Living S cells (control) Living R cells (control) Heat-killed S cells (control) Mixture of heat-killed S cells and living R cells Mouse dies Mouse diesMouse healthy Mouse healthy Living S cells EXPERIMENT RESULTS Figure 16.2
• In 1944, Oswald Avery, Maclyn McCarty, and Colin MacLeod announced that the transforming substance was DNA • Their conclusion was based on experimental evidence that only DNA worked in transforming harmless bacteria into pathogenic bacteria • Many biologists remained skeptical, mainly because little was known about DNA © 2011 Pearson Education, Inc.
Evidence That Viral DNA Can Program Cells • More evidence for DNA as the genetic material came from studies of viruses that infect bacteria • Such viruses, called bacteriophages (or phages), are widely used in molecular genetics research © 2011 Pearson Education, Inc. Animation: Phage T2 Reproductive Cycle
Figure 16.3 Phage head Tail sheath Tail fiber DNA Bacterial cell 100nm
• In 1952, Alfred Hershey and Martha Chase performed experiments showing that DNA is the genetic material of a phage known as T2 • To determine this, they designed an experiment showing that only one of the two components of T2 (DNA or protein) enters an E. coli cell during infection • They concluded that the injected DNA of the phage provides the genetic information © 2011 Pearson Education, Inc. Animation: Hershey-Chase Experiment
Figure 16.4-1 Bacterial cell Phage Batch 1: Radioactive sulfur (35 S) DNA Batch 2: Radioactive phosphorus (32 P) Radioactive DNA EXPERIMENT Radioactive protein
Figure 16.4-2 Bacterial cell Phage Batch 1: Radioactive sulfur (35 S) Radioactive protein DNA Batch 2: Radioactive phosphorus (32 P) Radioactive DNA Empty protein shell Phage DNA EXPERIMENT
Figure 16.4-3 Bacterial cell Phage Batch 1: Radioactive sulfur (35 S) Radioactive protein DNA Batch 2: Radioactive phosphorus (32 P) Radioactive DNA Empty protein shell Phage DNA Centrifuge Centrifuge Radioactivity (phage protein) in liquid Pellet (bacterial cells and contents) Pellet Radioactivity (phage DNA) in pellet EXPERIMENT
Additional Evidence That DNA Is the Genetic Material • It was known that DNA is a polymer of nucleotides, each consisting of a nitrogenous base, a sugar, and a phosphate group • In 1950, Erwin Chargaff reported that DNA composition varies from one species to the next • This evidence of diversity made DNA a more credible candidate for the genetic material © 2011 Pearson Education, Inc. Animation: DNA and RNA Structure
• Two findings became known as Chargaff’s rules – The base composition of DNA varies between species – In any species the number of A and T bases are equal and the number of G and C bases are equal • The basis for these rules was not understood until the discovery of the double helix © 2011 Pearson Education, Inc.
Figure 16.5 Sugar–phosphate backbone Nitrogenous bases Thymine (T) Adenine (A) Cytosine (C) Guanine (G) Nitrogenous base Phosphate DNA nucleotide Sugar (deoxyribose) 3′ end 5′ end
Building a Structural Model of DNA: Scientific Inquiry • After DNA was accepted as the genetic material, the challenge was to determine how its structure accounts for its role in heredity • Maurice Wilkins and Rosalind Franklin were using a technique called X-ray crystallography to study molecular structure • Franklin produced a picture of the DNA molecule using this technique © 2011 Pearson Education, Inc.
Figure 16.6 (a) Rosalind Franklin (b) Franklin’s X-ray diffraction photograph of DNA
Figure 16.6a (a) Rosalind Franklin
Figure 16.6b (b) Franklin’s X-ray diffraction photograph of DNA
• Franklin’s X-ray crystallographic images of DNA enabled Watson to deduce that DNA was helical • The X-ray images also enabled Watson to deduce the width of the helix and the spacing of the nitrogenous bases • The pattern in the photo suggested that the DNA molecule was made up of two strands, forming a double helix © 2011 Pearson Education, Inc. Animation: DNA Double Helix
Figure 16.7 3.4 nm 1 nm 0.34 nm Hydrogen bond (a) Key features of DNA structure Space-filling model (c)(b) Partial chemical structure 3′ end 5′ end 3′ end 5′ end T T A A G G C C C C C C C C C C C G G G G G G G G G T T T T T T A A A A A A
3.4 nm 1 nm 0.34 nm Hydrogen bond (a) Key features of DNA structure (b) Partial chemical structure 3′ end 5′ end 3′ end 5′ end T T A A G G C C C C C C C C C C C G G G G G G G G G T T T T T T A A A A A A Figure 16.7a
Figure 16.7b (c) Space-filling model
• Watson and Crick built models of a double helix to conform to the X-rays and chemistry of DNA • Franklin had concluded that there were two outer sugar-phosphate backbones, with the nitrogenous bases paired in the molecule’s interior • Watson built a model in which the backbones were antiparallel (their subunits run in opposite directions) © 2011 Pearson Education, Inc.
• At first, Watson and Crick thought the bases paired like with like (A with A, and so on), but such pairings did not result in a uniform width • Instead, pairing a purine with a pyrimidine resulted in a uniform width consistent with the X-ray data © 2011 Pearson Education, Inc.
Figure 16.UN01 Purine + purine: too wide Pyrimidine + pyrimidine: too narrow Purine + pyrimidine: width consistent with X-ray data
• Watson and Crick reasoned that the pairing was more specific, dictated by the base structures • They determined that adenine (A) paired only with thymine (T), and guanine (G) paired only with cytosine (C) • The Watson-Crick model explains Chargaff’s rules: in any organism the amount of A = T, and the amount of G = C © 2011 Pearson Education, Inc.
Figure 16.8 Sugar Sugar Sugar Sugar Adenine (A) Thymine (T) Guanine (G) Cytosine (C)
Concept 16.2: Many proteins work together in DNA replication and repair • The relationship between structure and function is manifest in the double helix • Watson and Crick noted that the specific base pairing suggested a possible copying mechanism for genetic material © 2011 Pearson Education, Inc.
The Basic Principle: Base Pairing to a Template Strand • Since the two strands of DNA are complementary, each strand acts as a template for building a new strand in replication • In DNA replication, the parent molecule unwinds, and two new daughter strands are built based on base-pairing rules © 2011 Pearson Education, Inc. Animation: DNA Replication Overview
Figure 16.9-1 (a) Parent molecule A A A T T T C C G G
Figure 16.9-2 (a) Parent molecule (b) Separation of strands A A A A A A T T T T T T C C C C G G G G
Figure 16.9-3 (a) Parent molecule (b) Separation of strands (c)“Daughter” DNA molecules, each consisting of one parental strand and one new strand A A A A A A A A A A A A T T T T T T T T T T T T C C C C C C C C G G G G G G G G
• Watson and Crick’s semiconservative model of replication predicts that when a double helix replicates, each daughter molecule will have one old strand (derived or “conserved” from the parent molecule) and one newly made strand • Competing models were the conservative model (the two parent strands rejoin) and the dispersive model (each strand is a mix of old and new) © 2011 Pearson Education, Inc.
Figure 16.10 (a) Conservative model (b) Semiconservative model (c) Dispersive model Parent cell First replication Second replication
• Experiments by Matthew Meselson and Franklin Stahl supported the semiconservative model • They labeled the nucleotides of the old strands with a heavy isotope of nitrogen, while any new nucleotides were labeled with a lighter isotope © 2011 Pearson Education, Inc.
• The first replication produced a band of hybrid DNA, eliminating the conservative model • A second replication produced both light and hybrid DNA, eliminating the dispersive model and supporting the semiconservative model © 2011 Pearson Education, Inc.
Figure 16.11 Bacteria cultured in medium with 15 N (heavy isotope) Bacteria transferred to medium with 14 N (lighter isotope) DNA sample centrifuged after first replication DNA sample centrifuged after second replication Less dense More dense Predictions: First replication Second replication Conservative model Semiconservative model Dispersive model 21 3 4 EXPERIMENT RESULTS CONCLUSION
Figure 16.11a Bacteria cultured in medium with 15 N (heavy isotope) Bacteria transferred to medium with 14 N (lighter isotope) DNA sample centrifuged after first replication DNA sample centrifuged after second replication Less dense More dense 21 3 4 EXPERIMENT RESULTS
Figure 16.11b Predictions: First replication Second replication Conservative model Semiconservative model Dispersive model CONCLUSION
DNA Replication: A Closer Look • The copying of DNA is remarkable in its speed and accuracy • More than a dozen enzymes and other proteins participate in DNA replication © 2011 Pearson Education, Inc.
Getting Started • Replication begins at particular sites called origins of replication, where the two DNA strands are separated, opening up a replication “bubble” • A eukaryotic chromosome may have hundreds or even thousands of origins of replication • Replication proceeds in both directions from each origin, until the entire molecule is copied © 2011 Pearson Education, Inc. Animation: Origins of Replication
Figure 16.12 (a) Origin of replication in an E. coli cell (b) Origins of replication in a eukaryotic cell Origin of replication Parental (template) strand Double- stranded DNA molecule Daughter (new) strand Replication fork Replication bubble Two daughter DNA molecules Origin of replication Double-stranded DNA molecule Parental (template) strand Daughter (new) strand Bubble Replication fork Two daughter DNA molecules 0.5µm 0.25µm
Figure 16.12a (a) Origin of replication in an E. coli cell Origin of replication Parental (template) strand Double- stranded DNA molecule Daughter (new) strand Replication fork Replication bubble Two daughter DNA molecules 0.5 µm
Figure 16.12b (b) Origins of replication in a eukaryotic cell Origin of replication Double-stranded DNA molecule Parental (template) strand Daughter (new) strand Bubble Replication fork Two daughter DNA molecules 0.25 µm
Figure 16.12c 0.5µm
Figure 16.12d 0.25µm
• At the end of each replication bubble is a replication fork, a Y-shaped region where new DNA strands are elongating • Helicases are enzymes that untwist the double helix at the replication forks • Single-strand binding proteins bind to and stabilize single-stranded DNA • Topoisomerase corrects “overwinding” ahead of replication forks by breaking, swiveling, and rejoining DNA strands © 2011 Pearson Education, Inc.
Figure 16.13 Topoisomerase Primase RNA primer Helicase Single-strand binding proteins 5′ 3′ 5′ 5′3′ 3′
• DNA polymerases cannot initiate synthesis of a polynucleotide; they can only add nucleotides to the 3′ end • The initial nucleotide strand is a short RNA primer © 2011 Pearson Education, Inc.
• An enzyme called primase can start an RNA chain from scratch and adds RNA nucleotides one at a time using the parental DNA as a template • The primer is short (5–10 nucleotides long), and the 3′ end serves as the starting point for the new DNA strand © 2011 Pearson Education, Inc.
Synthesizing a New DNA Strand • Enzymes called DNA polymerases catalyze the elongation of new DNA at a replication fork • Most DNA polymerases require a primer and a DNA template strand • The rate of elongation is about 500 nucleotides per second in bacteria and 50 per second in human cells © 2011 Pearson Education, Inc.
• Each nucleotide that is added to a growing DNA strand is a nucleoside triphosphate • dATP supplies adenine to DNA and is similar to the ATP of energy metabolism • The difference is in their sugars: dATP has deoxyribose while ATP has ribose • As each monomer of dATP joins the DNA strand, it loses two phosphate groups as a molecule of pyrophosphate © 2011 Pearson Education, Inc.
Figure 16.14 New strand Template strand Sugar Phosphate Base Nucleoside triphosphate DNA polymerase Pyrophosphate 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ OH OH OH P P i 2 P i P P P A A A A T T T T C C C C C C G G G G
Antiparallel Elongation • The antiparallel structure of the double helix affects replication • DNA polymerases add nucleotides only to the free 3′ end of a growing strand; therefore, a new DNA strand can elongate only in the 5′ to 3′ direction © 2011 Pearson Education, Inc.
• Along one template strand of DNA, the DNA polymerase synthesizes a leading strand continuously, moving toward the replication fork © 2011 Pearson Education, Inc. Animation: Leading Strand
Figure 16.15 Leading strand Lagging strand Overview Origin of replication Lagging strand Leading strand Primer Overall directions of replication Origin of replication RNA primer Sliding clamp DNA pol III Parental DNA 3′ 5′ 5′ 3′ 3′ 5′ 3′ 5′ 3′ 5′ 3′ 5′
Figure 16.15a Leading strand Lagging strand Overview Origin of replication Lagging strand Leading strand Primer Overall directions of replication
Origin of replication RNA primer Sliding clamp DNA pol III Parental DNA 3′ 5′ 5′ 3′ 3′ 5′ 3′ 5′ 3′ 5′ 3′ 5′ Figure 16.15b
• To elongate the other new strand, called the lagging strand, DNA polymerase must work in the direction away from the replication fork • The lagging strand is synthesized as a series of segments called Okazaki fragments, which are joined together by DNA ligase © 2011 Pearson Education, Inc. Animation: Lagging Strand
Origin of replication Overview Leading strand Leading strand Lagging strand Lagging strand Overall directions of replication Template strand RNA primer for fragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 Overall direction of replication 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′5′ 5′ 5′ 5′ 2 2 2 1 1 1 1 1 2 1 Figure 16.16
Figure 16.16a Origin of replication Overview Leading strand Leading strand Lagging strand Lagging strand Overall directions of replication 1 2
Figure 16.16b-1 Template strand 3′ 3′5′ 5′
Figure 16.16b-2 Template strand RNA primer for fragment 1 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 1
Figure 16.16b-3 Template strand RNA primer for fragment 1 Okazaki fragment 1 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 1 1
Figure 16.16b-4 Template strand RNA primer for fragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 2 1 1 1
Figure 16.16b-5 Template strand RNA primer for fragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′5′ 2 2 1 1 1 1
Figure 16.16b-6 Template strand RNA primer for fragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 Overall direction of replication 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′5′ 5′ 2 2 2 1 1 1 1 1
Figure 16.17 Overview Leading strand Origin of replication Lagging strand Leading strandLagging strand Overall directions of replicationLeading strand DNA pol III DNA pol III Lagging strand DNA pol I DNA ligase Primer Primase Parental DNA 5′ 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ 3′3 2 1 4
Figure 16.17a Overview Leading strand Origin of replication Lagging strand Leading strandLagging strand Overall directions of replication Leading strand DNA pol III Primer Primase Parental DNA 5′ 5′3′ 3′ 3′
Overview Leading strand Origin of replication Lagging strand Leading strandLagging strand Overall directions of replicationLeading strand Primer DNA pol III DNA pol I Lagging strand DNA ligase 5′ 5′ 5′ 3′ 3′ 3′ 3 4 2 1 Figure 16.17b
The DNA Replication Complex • The proteins that participate in DNA replication form a large complex, a “DNA replication machine” • The DNA replication machine may be stationary during the replication process • Recent studies support a model in which DNA polymerase molecules “reel in” parental DNA and “extrude” newly made daughter DNA molecules © 2011 Pearson Education, Inc. Animation: DNA Replication Review
Figure 16.18 Parental DNA DNA pol III Leading strand Connecting protein Helicase Lagging strandDNA pol III Lagging strand template 5′ 5′ 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ 3′ 3′
Proofreading and Repairing DNA • DNA polymerases proofread newly made DNA, replacing any incorrect nucleotides • In mismatch repair of DNA, repair enzymes correct errors in base pairing • DNA can be damaged by exposure to harmful chemical or physical agents such as cigarette smoke and X-rays; it can also undergo spontaneous changes • In nucleotide excision repair, a nuclease cuts out and replaces damaged stretches of DNA © 2011 Pearson Education, Inc.
Figure 16.19 Nuclease DNA polymerase DNA ligase 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′
Evolutionary Significance of Altered DNA Nucleotides • Error rate after proofreading repair is low but not zero • Sequence changes may become permanent and can be passed on to the next generation • These changes (mutations) are the source of the genetic variation upon which natural selection operates © 2011 Pearson Education, Inc.
Replicating the Ends of DNA Molecules • Limitations of DNA polymerase create problems for the linear DNA of eukaryotic chromosomes • The usual replication machinery provides no way to complete the 5′ ends, so repeated rounds of replication produce shorter DNA molecules with uneven ends • This is not a problem for prokaryotes, most of which have circular chromosomes © 2011 Pearson Education, Inc.
Figure 16.20 Ends of parental DNA strands Leading strand Lagging strand Last fragment Next-to-last fragment Lagging strand RNA primer Parental strand Removal of primers and replacement with DNA where a 3′ end is available Second round of replication Further rounds of replication New leading strand New lagging strand Shorter and shorter daughter molecules 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′
Figure 16.20a Ends of parental DNA strands Leading strand Lagging strand Last fragment Next-to-last fragment Lagging strand RNA primer Parental strand Removal of primers and replacement with DNA where a 3′ end is available 3′ 3′ 3′ 5′ 5′ 5′
Figure 16.20b Second round of replication Further rounds of replication New leading strand New lagging strand Shorter and shorter daughter molecules 3′ 3′ 3′ 5′ 5′ 5′
• Eukaryotic chromosomal DNA molecules have special nucleotide sequences at their ends called telomeres • Telomeres do not prevent the shortening of DNA molecules, but they do postpone the erosion of genes near the ends of DNA molecules • It has been proposed that the shortening of telomeres is connected to aging © 2011 Pearson Education, Inc.
Figure 16.21 1 µm
• If chromosomes of germ cells became shorter in every cell cycle, essential genes would eventually be missing from the gametes they produce • An enzyme called telomerase catalyzes the lengthening of telomeres in germ cells © 2011 Pearson Education, Inc.
• The shortening of telomeres might protect cells from cancerous growth by limiting the number of cell divisions • There is evidence of telomerase activity in cancer cells, which may allow cancer cells to persist © 2011 Pearson Education, Inc.
Concept 16.3 A chromosome consists of a DNA molecule packed together with proteins • The bacterial chromosome is a double-stranded, circular DNA molecule associated with a small amount of protein • Eukaryotic chromosomes have linear DNA molecules associated with a large amount of protein • In a bacterium, the DNA is “supercoiled” and found in a region of the cell called the nucleoid © 2011 Pearson Education, Inc.
• Chromatin, a complex of DNA and protein, is found in the nucleus of eukaryotic cells • Chromosomes fit into the nucleus through an elaborate, multilevel system of packing © 2011 Pearson Education, Inc. Animation: DNA Packing
Figure 16.22a DNA double helix (2 nm in diameter) DNA, the double helix Nucleosome (10 nm in diameter) Histones Histones Histone tail H1 Nucleosomes, or “beads on a string” (10-nm fiber)
Figure 16.22b 30-nm fiber 30-nm fiber Loops Scaffold 300-nm fiber Chromatid (700 nm) Replicated chromosome (1,400 nm) Looped domains (300-nm fiber) Metaphase chromosome
Figure 16.22c DNA double helix (2 nm in diameter)
Figure 16.22d Nucleosome (10 nm in diameter)
Figure 16.22e 30-nm fiber
Figure 16.22f Loops Scaffold
Figure 16.22g Chromatid (700 nm)
• Chromatin undergoes changes in packing during the cell cycle • At interphase, some chromatin is organized into a 10-nm fiber, but much is compacted into a 30-nm fiber, through folding and looping • Though interphase chromosomes are not highly condensed, they still occupy specific restricted regions in the nucleus © 2011 Pearson Education, Inc.
Figure 16.23 5µm
Figure 16.23a
Figure 16.23b
Figure 16.23c 5µm
• Most chromatin is loosely packed in the nucleus during interphase and condenses prior to mitosis • Loosely packed chromatin is called euchromatin • During interphase a few regions of chromatin (centromeres and telomeres) are highly condensed into heterochromatin • Dense packing of the heterochromatin makes it difficult for the cell to express genetic information coded in these regions © 2011 Pearson Education, Inc.
• Histones can undergo chemical modifications that result in changes in chromatin organization © 2011 Pearson Education, Inc.
Figure 16.UN02 Sugar-phosphate backbone Nitrogenous bases Hydrogen bond G G G G C C C C A A A A T T T T
Figure 16.UN03 DNA pol III synthesizes leading strand continuously Parental DNA DNA pol III starts DNA synthesis at 3′ end of primer, continues in 5′ → 3′ direction Origin of replication Helicase Primase synthesizes a short RNA primer DNA pol I replaces the RNA primer with DNA nucleotides 3′ 3′ 3′ 5′ 5′ 5′ 5′ Lagging strand synthesized in short Okazaki fragments, later joined by DNA ligase
Figure 16.UN04
Figure 16.UN05
Figure 16.UN06
Figure 16.UN07

More Related Content

PPT
14 mendel and the gene idea
bykindarspirit
 
PPT
Ch 14: Mendel and the Gene Idea
byveneethmathew
 
PPT
Ch 15: The Chromosomal Basis of Inheritance
byveneethmathew
 
PPT
21 lecture genome_and_evolution
byveneethmathew
 
PPT
20 lecture biotech
byveneethmathew
 
PPT
Ch 17: From Gene to Protein
byveneethmathew
 
PPT
22 lecture descent_with_modification
byveneethmathew
 
PPT
18 Regulation of Gene Expression
bykindarspirit
 
14 mendel and the gene idea
bykindarspirit
 
Ch 14: Mendel and the Gene Idea
byveneethmathew
 
Ch 15: The Chromosomal Basis of Inheritance
byveneethmathew
 
21 lecture genome_and_evolution
byveneethmathew
 
20 lecture biotech
byveneethmathew
 
Ch 17: From Gene to Protein
byveneethmathew
 
22 lecture descent_with_modification
byveneethmathew
 
18 Regulation of Gene Expression
bykindarspirit
 

What's hot

PPT
Ch 13: Meiosis and Sexual Life Cycles
byveneethmathew
 
PPT
16 the molecular basis of inheritance
bykindarspirit
 
PPT
23 lecture evolution_populations
byveneethmathew
 
PPT
Ch 12: Cell Cycle
byveneethmathew
 
PPT
13 meiosis and sexual life cycles
bykindarspirit
 
PPT
25 lecture history_of_life
byveneethmathew
 
PPT
17 - From Gene to Protein
bykindarspirit
 
PPT
19 - Viruses
bykindarspirit
 
PPT
27 lecture bacteria
byveneethmathew
 
PPT
Ch 10: Photosynthesis
byveneethmathew
 
PPT
Biology in Focus - Chapter 11
bympattani
 
PPT
19 lecture viruses
byveneethmathew
 
PPT
24 lecture origin_of_species
byveneethmathew
 
PPT
12 the cell cycle
bykindarspirit
 
PPT
Chapter52
byuv5
 
PPT
21 genomes and their evolution
bykindarspirit
 
PPT
23 the evolution of populations
bykindarspirit
 
PPT
26 lecture phylogeny
byveneethmathew
 
PPT
Biology in Focus - Chapter 13
bympattani
 
PPT
Chapter 48: Nuerons
byAngel Vega
 
Ch 13: Meiosis and Sexual Life Cycles
byveneethmathew
 
16 the molecular basis of inheritance
bykindarspirit
 
23 lecture evolution_populations
byveneethmathew
 
Ch 12: Cell Cycle
byveneethmathew
 
13 meiosis and sexual life cycles
bykindarspirit
 
25 lecture history_of_life
byveneethmathew
 
17 - From Gene to Protein
bykindarspirit
 
19 - Viruses
bykindarspirit
 
27 lecture bacteria
byveneethmathew
 
Ch 10: Photosynthesis
byveneethmathew
 
Biology in Focus - Chapter 11
bympattani
 
19 lecture viruses
byveneethmathew
 
24 lecture origin_of_species
byveneethmathew
 
12 the cell cycle
bykindarspirit
 
Chapter52
byuv5
 
21 genomes and their evolution
bykindarspirit
 
23 the evolution of populations
bykindarspirit
 
26 lecture phylogeny
byveneethmathew
 
Biology in Focus - Chapter 13
bympattani
 
Chapter 48: Nuerons
byAngel Vega
 

Similar to Ch 16: The Molecular Basis of Inheritance

PPT
Chapter 16.ppt untuk persiapn olimpiade sma
byYuliaNingsih95
 
PPT
Dezoksiribonukleinkislotlar____123456.ppt
byrakhmonovmurodjon7
 
PPT
Ap Chapter 16
bysmithbio
 
PPT
16-molecularinheritance lecture text.ppt
bykhalidmr1830
 
PPT
Campbell Recee Biology- Molecular Bases of Inheritance
byNergizDemirer
 
PPT
Dna History And Replication Review
byCrystal Wood
 
PPTX
L5 DNA structure and replication.pptx
byAbdulkarim803288
 
PPT
Chapter 16 molecular inheritance
byHeather Fogell
 
PPT
16 molecularinheritance text
byRv26121972
 
PPT
The molecular basis of inheritance
bytanzeem khan
 
PDF
13_Lecture_Presentakkkkkkktion 1 ppt.pdf
byvaradasakore031
 
PPT
Chapter 16: Molecular Basis of Inheritance
byAngel Vega
 
PPT
Chapter 16
byktanaka2
 
PPT
Chapter 16
byktanaka2
 
PPT
Dn ato protein
byAndrew McCaskill
 
PDF
Molecular basis of inheritance
byV.s. Malik
 
PPTX
Unit 1 genetics nucleic acids dna
byjane namane
 
PPTX
Unit 1 genetics nucleic acids dna
byDudrah Moyo
 
PPTX
Unit 1 genetics nucleic acids dna
byThabo Bafana
 
PPTX
Unit 1 genetics nucleic acids dna
byseleka moema
 
Chapter 16.ppt untuk persiapn olimpiade sma
byYuliaNingsih95
 
Dezoksiribonukleinkislotlar____123456.ppt
byrakhmonovmurodjon7
 
Ap Chapter 16
bysmithbio
 
16-molecularinheritance lecture text.ppt
bykhalidmr1830
 
Campbell Recee Biology- Molecular Bases of Inheritance
byNergizDemirer
 
Dna History And Replication Review
byCrystal Wood
 
L5 DNA structure and replication.pptx
byAbdulkarim803288
 
Chapter 16 molecular inheritance
byHeather Fogell
 
16 molecularinheritance text
byRv26121972
 
The molecular basis of inheritance
bytanzeem khan
 
13_Lecture_Presentakkkkkkktion 1 ppt.pdf
byvaradasakore031
 
Chapter 16: Molecular Basis of Inheritance
byAngel Vega
 
Chapter 16
byktanaka2
 
Chapter 16
byktanaka2
 
Dn ato protein
byAndrew McCaskill
 
Molecular basis of inheritance
byV.s. Malik
 
Unit 1 genetics nucleic acids dna
byjane namane
 
Unit 1 genetics nucleic acids dna
byDudrah Moyo
 
Unit 1 genetics nucleic acids dna
byThabo Bafana
 
Unit 1 genetics nucleic acids dna
byseleka moema
 

More from veneethmathew

PPT
Ch 11: Cell Communication
byveneethmathew
 
PPT
Ch 8: Introduction to Metabolism
byveneethmathew
 
PPT
Ch 7: Membrane Structure and Function
byveneethmathew
 
PPT
Ch 6: A Tour of the Cell
byveneethmathew
 
PPT
Ch 5: The Structure and Function of Large Biological Molecules
byveneethmathew
 
PPT
Ch 4: Carbon and Diversity
byveneethmathew
 
PPT
Ch 3: Water and Life
byveneethmathew
 
PPT
Ch 2: The Chemical Context of Life
byveneethmathew
 
PPT
Ch 1: Themes in the Study of Life
byveneethmathew
 
Ch 11: Cell Communication
byveneethmathew
 
Ch 8: Introduction to Metabolism
byveneethmathew
 
Ch 7: Membrane Structure and Function
byveneethmathew
 
Ch 6: A Tour of the Cell
byveneethmathew
 
Ch 5: The Structure and Function of Large Biological Molecules
byveneethmathew
 
Ch 4: Carbon and Diversity
byveneethmathew
 
Ch 3: Water and Life
byveneethmathew
 
Ch 2: The Chemical Context of Life
byveneethmathew
 
Ch 1: Themes in the Study of Life
byveneethmathew
 

Ch 16: The Molecular Basis of Inheritance

  • 1.
    LECTURE PRESENTATIONS For CAMPBELLBIOLOGY, NINTH EDITION Jane B. Reece, Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson © 2011 Pearson Education, Inc. Lectures by Erin Barley Kathleen Fitzpatrick The Molecular Basis of Inheritance Chapter 16
  • 2.
    Overview: Life’s OperatingInstructions • In 1953, James Watson and Francis Crick introduced an elegant double-helical model for the structure of deoxyribonucleic acid, or DNA • DNA, the substance of inheritance, is the most celebrated molecule of our time • Hereditary information is encoded in DNA and reproduced in all cells of the body • This DNA program directs the development of biochemical, anatomical, physiological, and (to some extent) behavioral traits © 2011 Pearson Education, Inc.
  • 3.
  • 4.
    Concept 16.1: DNAis the genetic material • Early in the 20th century, the identification of the molecules of inheritance loomed as a major challenge to biologists © 2011 Pearson Education, Inc.
  • 5.
    The Search forthe Genetic Material: Scientific Inquiry • When T. H. Morgan’s group showed that genes are located on chromosomes, the two components of chromosomes—DNA and protein—became candidates for the genetic material • The key factor in determining the genetic material was choosing appropriate experimental organisms • The role of DNA in heredity was first discovered by studying bacteria and the viruses that infect them © 2011 Pearson Education, Inc.
  • 6.
    Evidence That DNACan Transform Bacteria • The discovery of the genetic role of DNA began with research by Frederick Griffith in 1928 • Griffith worked with two strains of a bacterium, one pathogenic and one harmless © 2011 Pearson Education, Inc.
  • 7.
    • When hemixed heat-killed remains of the pathogenic strain with living cells of the harmless strain, some living cells became pathogenic • He called this phenomenon transformation, now defined as a change in genotype and phenotype due to assimilation of foreign DNA © 2011 Pearson Education, Inc.
  • 8.
    Living S cells (control) LivingR cells (control) Heat-killed S cells (control) Mixture of heat-killed S cells and living R cells Mouse dies Mouse diesMouse healthy Mouse healthy Living S cells EXPERIMENT RESULTS Figure 16.2
  • 9.
    • In 1944,Oswald Avery, Maclyn McCarty, and Colin MacLeod announced that the transforming substance was DNA • Their conclusion was based on experimental evidence that only DNA worked in transforming harmless bacteria into pathogenic bacteria • Many biologists remained skeptical, mainly because little was known about DNA © 2011 Pearson Education, Inc.
  • 10.
    Evidence That ViralDNA Can Program Cells • More evidence for DNA as the genetic material came from studies of viruses that infect bacteria • Such viruses, called bacteriophages (or phages), are widely used in molecular genetics research © 2011 Pearson Education, Inc. Animation: Phage T2 Reproductive Cycle
  • 11.
  • 12.
    • In 1952,Alfred Hershey and Martha Chase performed experiments showing that DNA is the genetic material of a phage known as T2 • To determine this, they designed an experiment showing that only one of the two components of T2 (DNA or protein) enters an E. coli cell during infection • They concluded that the injected DNA of the phage provides the genetic information © 2011 Pearson Education, Inc. Animation: Hershey-Chase Experiment
  • 13.
    Figure 16.4-1 Bacterial cell Phage Batch1: Radioactive sulfur (35 S) DNA Batch 2: Radioactive phosphorus (32 P) Radioactive DNA EXPERIMENT Radioactive protein
  • 14.
    Figure 16.4-2 Bacterial cell Phage Batch1: Radioactive sulfur (35 S) Radioactive protein DNA Batch 2: Radioactive phosphorus (32 P) Radioactive DNA Empty protein shell Phage DNA EXPERIMENT
  • 15.
    Figure 16.4-3 Bacterial cell Phage Batch1: Radioactive sulfur (35 S) Radioactive protein DNA Batch 2: Radioactive phosphorus (32 P) Radioactive DNA Empty protein shell Phage DNA Centrifuge Centrifuge Radioactivity (phage protein) in liquid Pellet (bacterial cells and contents) Pellet Radioactivity (phage DNA) in pellet EXPERIMENT
  • 16.
    Additional Evidence ThatDNA Is the Genetic Material • It was known that DNA is a polymer of nucleotides, each consisting of a nitrogenous base, a sugar, and a phosphate group • In 1950, Erwin Chargaff reported that DNA composition varies from one species to the next • This evidence of diversity made DNA a more credible candidate for the genetic material © 2011 Pearson Education, Inc. Animation: DNA and RNA Structure
  • 17.
    • Two findingsbecame known as Chargaff’s rules – The base composition of DNA varies between species – In any species the number of A and T bases are equal and the number of G and C bases are equal • The basis for these rules was not understood until the discovery of the double helix © 2011 Pearson Education, Inc.
  • 18.
    Figure 16.5 Sugar–phosphate backbone Nitrogenous bases Thymine(T) Adenine (A) Cytosine (C) Guanine (G) Nitrogenous base Phosphate DNA nucleotide Sugar (deoxyribose) 3′ end 5′ end
  • 19.
    Building a StructuralModel of DNA: Scientific Inquiry • After DNA was accepted as the genetic material, the challenge was to determine how its structure accounts for its role in heredity • Maurice Wilkins and Rosalind Franklin were using a technique called X-ray crystallography to study molecular structure • Franklin produced a picture of the DNA molecule using this technique © 2011 Pearson Education, Inc.
  • 20.
    Figure 16.6 (a) RosalindFranklin (b) Franklin’s X-ray diffraction photograph of DNA
  • 21.
  • 22.
    Figure 16.6b (b) Franklin’sX-ray diffraction photograph of DNA
  • 23.
    • Franklin’s X-raycrystallographic images of DNA enabled Watson to deduce that DNA was helical • The X-ray images also enabled Watson to deduce the width of the helix and the spacing of the nitrogenous bases • The pattern in the photo suggested that the DNA molecule was made up of two strands, forming a double helix © 2011 Pearson Education, Inc. Animation: DNA Double Helix
  • 24.
    Figure 16.7 3.4 nm 1nm 0.34 nm Hydrogen bond (a) Key features of DNA structure Space-filling model (c)(b) Partial chemical structure 3′ end 5′ end 3′ end 5′ end T T A A G G C C C C C C C C C C C G G G G G G G G G T T T T T T A A A A A A
  • 25.
    3.4 nm 1 nm 0.34nm Hydrogen bond (a) Key features of DNA structure (b) Partial chemical structure 3′ end 5′ end 3′ end 5′ end T T A A G G C C C C C C C C C C C G G G G G G G G G T T T T T T A A A A A A Figure 16.7a
  • 26.
  • 27.
    • Watson andCrick built models of a double helix to conform to the X-rays and chemistry of DNA • Franklin had concluded that there were two outer sugar-phosphate backbones, with the nitrogenous bases paired in the molecule’s interior • Watson built a model in which the backbones were antiparallel (their subunits run in opposite directions) © 2011 Pearson Education, Inc.
  • 28.
    • At first,Watson and Crick thought the bases paired like with like (A with A, and so on), but such pairings did not result in a uniform width • Instead, pairing a purine with a pyrimidine resulted in a uniform width consistent with the X-ray data © 2011 Pearson Education, Inc.
  • 29.
    Figure 16.UN01 Purine +purine: too wide Pyrimidine + pyrimidine: too narrow Purine + pyrimidine: width consistent with X-ray data
  • 30.
    • Watson andCrick reasoned that the pairing was more specific, dictated by the base structures • They determined that adenine (A) paired only with thymine (T), and guanine (G) paired only with cytosine (C) • The Watson-Crick model explains Chargaff’s rules: in any organism the amount of A = T, and the amount of G = C © 2011 Pearson Education, Inc.
  • 31.
    Figure 16.8 Sugar Sugar Sugar Sugar Adenine (A)Thymine (T) Guanine (G) Cytosine (C)
  • 32.
    Concept 16.2: Manyproteins work together in DNA replication and repair • The relationship between structure and function is manifest in the double helix • Watson and Crick noted that the specific base pairing suggested a possible copying mechanism for genetic material © 2011 Pearson Education, Inc.
  • 33.
    The Basic Principle:Base Pairing to a Template Strand • Since the two strands of DNA are complementary, each strand acts as a template for building a new strand in replication • In DNA replication, the parent molecule unwinds, and two new daughter strands are built based on base-pairing rules © 2011 Pearson Education, Inc. Animation: DNA Replication Overview
  • 34.
    Figure 16.9-1 (a) Parentmolecule A A A T T T C C G G
  • 35.
    Figure 16.9-2 (a) Parentmolecule (b) Separation of strands A A A A A A T T T T T T C C C C G G G G
  • 36.
    Figure 16.9-3 (a) Parentmolecule (b) Separation of strands (c)“Daughter” DNA molecules, each consisting of one parental strand and one new strand A A A A A A A A A A A A T T T T T T T T T T T T C C C C C C C C G G G G G G G G
  • 37.
    • Watson andCrick’s semiconservative model of replication predicts that when a double helix replicates, each daughter molecule will have one old strand (derived or “conserved” from the parent molecule) and one newly made strand • Competing models were the conservative model (the two parent strands rejoin) and the dispersive model (each strand is a mix of old and new) © 2011 Pearson Education, Inc.
  • 38.
    Figure 16.10 (a) Conservative model (b)Semiconservative model (c) Dispersive model Parent cell First replication Second replication
  • 39.
    • Experiments byMatthew Meselson and Franklin Stahl supported the semiconservative model • They labeled the nucleotides of the old strands with a heavy isotope of nitrogen, while any new nucleotides were labeled with a lighter isotope © 2011 Pearson Education, Inc.
  • 40.
    • The firstreplication produced a band of hybrid DNA, eliminating the conservative model • A second replication produced both light and hybrid DNA, eliminating the dispersive model and supporting the semiconservative model © 2011 Pearson Education, Inc.
  • 41.
    Figure 16.11 Bacteria cultured in mediumwith 15 N (heavy isotope) Bacteria transferred to medium with 14 N (lighter isotope) DNA sample centrifuged after first replication DNA sample centrifuged after second replication Less dense More dense Predictions: First replication Second replication Conservative model Semiconservative model Dispersive model 21 3 4 EXPERIMENT RESULTS CONCLUSION
  • 42.
    Figure 16.11a Bacteria cultured in mediumwith 15 N (heavy isotope) Bacteria transferred to medium with 14 N (lighter isotope) DNA sample centrifuged after first replication DNA sample centrifuged after second replication Less dense More dense 21 3 4 EXPERIMENT RESULTS
  • 43.
    Figure 16.11b Predictions: Firstreplication Second replication Conservative model Semiconservative model Dispersive model CONCLUSION
  • 44.
    DNA Replication: ACloser Look • The copying of DNA is remarkable in its speed and accuracy • More than a dozen enzymes and other proteins participate in DNA replication © 2011 Pearson Education, Inc.
  • 45.
    Getting Started • Replicationbegins at particular sites called origins of replication, where the two DNA strands are separated, opening up a replication “bubble” • A eukaryotic chromosome may have hundreds or even thousands of origins of replication • Replication proceeds in both directions from each origin, until the entire molecule is copied © 2011 Pearson Education, Inc. Animation: Origins of Replication
  • 46.
    Figure 16.12 (a) Originof replication in an E. coli cell (b) Origins of replication in a eukaryotic cell Origin of replication Parental (template) strand Double- stranded DNA molecule Daughter (new) strand Replication fork Replication bubble Two daughter DNA molecules Origin of replication Double-stranded DNA molecule Parental (template) strand Daughter (new) strand Bubble Replication fork Two daughter DNA molecules 0.5µm 0.25µm
  • 47.
    Figure 16.12a (a) Originof replication in an E. coli cell Origin of replication Parental (template) strand Double- stranded DNA molecule Daughter (new) strand Replication fork Replication bubble Two daughter DNA molecules 0.5 µm
  • 48.
    Figure 16.12b (b) Originsof replication in a eukaryotic cell Origin of replication Double-stranded DNA molecule Parental (template) strand Daughter (new) strand Bubble Replication fork Two daughter DNA molecules 0.25 µm
  • 49.
  • 50.
  • 51.
    • At theend of each replication bubble is a replication fork, a Y-shaped region where new DNA strands are elongating • Helicases are enzymes that untwist the double helix at the replication forks • Single-strand binding proteins bind to and stabilize single-stranded DNA • Topoisomerase corrects “overwinding” ahead of replication forks by breaking, swiveling, and rejoining DNA strands © 2011 Pearson Education, Inc.
  • 52.
  • 53.
    • DNA polymerasescannot initiate synthesis of a polynucleotide; they can only add nucleotides to the 3′ end • The initial nucleotide strand is a short RNA primer © 2011 Pearson Education, Inc.
  • 54.
    • An enzymecalled primase can start an RNA chain from scratch and adds RNA nucleotides one at a time using the parental DNA as a template • The primer is short (5–10 nucleotides long), and the 3′ end serves as the starting point for the new DNA strand © 2011 Pearson Education, Inc.
  • 55.
    Synthesizing a NewDNA Strand • Enzymes called DNA polymerases catalyze the elongation of new DNA at a replication fork • Most DNA polymerases require a primer and a DNA template strand • The rate of elongation is about 500 nucleotides per second in bacteria and 50 per second in human cells © 2011 Pearson Education, Inc.
  • 56.
    • Each nucleotidethat is added to a growing DNA strand is a nucleoside triphosphate • dATP supplies adenine to DNA and is similar to the ATP of energy metabolism • The difference is in their sugars: dATP has deoxyribose while ATP has ribose • As each monomer of dATP joins the DNA strand, it loses two phosphate groups as a molecule of pyrophosphate © 2011 Pearson Education, Inc.
  • 57.
    Figure 16.14 New strandTemplate strand Sugar Phosphate Base Nucleoside triphosphate DNA polymerase Pyrophosphate 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ OH OH OH P P i 2 P i P P P A A A A T T T T C C C C C C G G G G
  • 58.
    Antiparallel Elongation • Theantiparallel structure of the double helix affects replication • DNA polymerases add nucleotides only to the free 3′ end of a growing strand; therefore, a new DNA strand can elongate only in the 5′ to 3′ direction © 2011 Pearson Education, Inc.
  • 59.
    • Along onetemplate strand of DNA, the DNA polymerase synthesizes a leading strand continuously, moving toward the replication fork © 2011 Pearson Education, Inc. Animation: Leading Strand
  • 60.
    Figure 16.15 Leading strand Lagging strand Overview Origin ofreplication Lagging strand Leading strand Primer Overall directions of replication Origin of replication RNA primer Sliding clamp DNA pol III Parental DNA 3′ 5′ 5′ 3′ 3′ 5′ 3′ 5′ 3′ 5′ 3′ 5′
  • 61.
    Figure 16.15a Leading strand Lagging strand Overview Origin ofreplication Lagging strand Leading strand Primer Overall directions of replication
  • 62.
    Origin of replication RNA primer Slidingclamp DNA pol III Parental DNA 3′ 5′ 5′ 3′ 3′ 5′ 3′ 5′ 3′ 5′ 3′ 5′ Figure 16.15b
  • 63.
    • To elongatethe other new strand, called the lagging strand, DNA polymerase must work in the direction away from the replication fork • The lagging strand is synthesized as a series of segments called Okazaki fragments, which are joined together by DNA ligase © 2011 Pearson Education, Inc. Animation: Lagging Strand
  • 64.
    Origin of replication Overview Leading strand Leading strand Lagging strand Laggingstrand Overall directions of replication Template strand RNA primer for fragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 Overall direction of replication 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′5′ 5′ 5′ 5′ 2 2 2 1 1 1 1 1 2 1 Figure 16.16
  • 65.
    Figure 16.16a Origin ofreplication Overview Leading strand Leading strand Lagging strand Lagging strand Overall directions of replication 1 2
  • 66.
  • 67.
    Figure 16.16b-2 Template strand RNA primer forfragment 1 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 1
  • 68.
    Figure 16.16b-3 Template strand RNA primer forfragment 1 Okazaki fragment 1 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 1 1
  • 69.
    Figure 16.16b-4 Template strand RNA primer forfragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 2 1 1 1
  • 70.
    Figure 16.16b-5 Template strand RNA primer forfragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′5′ 2 2 1 1 1 1
  • 71.
    Figure 16.16b-6 Template strand RNA primer forfragment 1 Okazaki fragment 1 RNA primer for fragment 2 Okazaki fragment 2 Overall direction of replication 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′ 5′5′ 5′ 2 2 2 1 1 1 1 1
  • 72.
    Figure 16.17 Overview Leading strand Origin of replicationLagging strand Leading strandLagging strand Overall directions of replicationLeading strand DNA pol III DNA pol III Lagging strand DNA pol I DNA ligase Primer Primase Parental DNA 5′ 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ 3′3 2 1 4
  • 73.
    Figure 16.17a Overview Leading strand Origin of replicationLagging strand Leading strandLagging strand Overall directions of replication Leading strand DNA pol III Primer Primase Parental DNA 5′ 5′3′ 3′ 3′
  • 74.
    Overview Leading strand Origin of replication Lagging strand Leading strandLagging strandOverall directions of replicationLeading strand Primer DNA pol III DNA pol I Lagging strand DNA ligase 5′ 5′ 5′ 3′ 3′ 3′ 3 4 2 1 Figure 16.17b
  • 75.
    The DNA ReplicationComplex • The proteins that participate in DNA replication form a large complex, a “DNA replication machine” • The DNA replication machine may be stationary during the replication process • Recent studies support a model in which DNA polymerase molecules “reel in” parental DNA and “extrude” newly made daughter DNA molecules © 2011 Pearson Education, Inc. Animation: DNA Replication Review
  • 76.
    Figure 16.18 Parental DNA DNApol III Leading strand Connecting protein Helicase Lagging strandDNA pol III Lagging strand template 5′ 5′ 5′ 5′ 5′ 5′ 3′ 3′ 3′ 3′ 3′ 3′
  • 77.
    Proofreading and RepairingDNA • DNA polymerases proofread newly made DNA, replacing any incorrect nucleotides • In mismatch repair of DNA, repair enzymes correct errors in base pairing • DNA can be damaged by exposure to harmful chemical or physical agents such as cigarette smoke and X-rays; it can also undergo spontaneous changes • In nucleotide excision repair, a nuclease cuts out and replaces damaged stretches of DNA © 2011 Pearson Education, Inc.
  • 78.
  • 79.
    Evolutionary Significance ofAltered DNA Nucleotides • Error rate after proofreading repair is low but not zero • Sequence changes may become permanent and can be passed on to the next generation • These changes (mutations) are the source of the genetic variation upon which natural selection operates © 2011 Pearson Education, Inc.
  • 80.
    Replicating the Endsof DNA Molecules • Limitations of DNA polymerase create problems for the linear DNA of eukaryotic chromosomes • The usual replication machinery provides no way to complete the 5′ ends, so repeated rounds of replication produce shorter DNA molecules with uneven ends • This is not a problem for prokaryotes, most of which have circular chromosomes © 2011 Pearson Education, Inc.
  • 81.
    Figure 16.20 Ends ofparental DNA strands Leading strand Lagging strand Last fragment Next-to-last fragment Lagging strand RNA primer Parental strand Removal of primers and replacement with DNA where a 3′ end is available Second round of replication Further rounds of replication New leading strand New lagging strand Shorter and shorter daughter molecules 3′ 3′ 3′ 3′ 3′ 5′ 5′ 5′ 5′ 5′
  • 82.
    Figure 16.20a Ends ofparental DNA strands Leading strand Lagging strand Last fragment Next-to-last fragment Lagging strand RNA primer Parental strand Removal of primers and replacement with DNA where a 3′ end is available 3′ 3′ 3′ 5′ 5′ 5′
  • 83.
    Figure 16.20b Second round ofreplication Further rounds of replication New leading strand New lagging strand Shorter and shorter daughter molecules 3′ 3′ 3′ 5′ 5′ 5′
  • 84.
    • Eukaryotic chromosomalDNA molecules have special nucleotide sequences at their ends called telomeres • Telomeres do not prevent the shortening of DNA molecules, but they do postpone the erosion of genes near the ends of DNA molecules • It has been proposed that the shortening of telomeres is connected to aging © 2011 Pearson Education, Inc.
  • 85.
  • 86.
    • If chromosomesof germ cells became shorter in every cell cycle, essential genes would eventually be missing from the gametes they produce • An enzyme called telomerase catalyzes the lengthening of telomeres in germ cells © 2011 Pearson Education, Inc.
  • 87.
    • The shorteningof telomeres might protect cells from cancerous growth by limiting the number of cell divisions • There is evidence of telomerase activity in cancer cells, which may allow cancer cells to persist © 2011 Pearson Education, Inc.
  • 88.
    Concept 16.3 Achromosome consists of a DNA molecule packed together with proteins • The bacterial chromosome is a double-stranded, circular DNA molecule associated with a small amount of protein • Eukaryotic chromosomes have linear DNA molecules associated with a large amount of protein • In a bacterium, the DNA is “supercoiled” and found in a region of the cell called the nucleoid © 2011 Pearson Education, Inc.
  • 89.
    • Chromatin, acomplex of DNA and protein, is found in the nucleus of eukaryotic cells • Chromosomes fit into the nucleus through an elaborate, multilevel system of packing © 2011 Pearson Education, Inc. Animation: DNA Packing
  • 90.
    Figure 16.22a DNA doublehelix (2 nm in diameter) DNA, the double helix Nucleosome (10 nm in diameter) Histones Histones Histone tail H1 Nucleosomes, or “beads on a string” (10-nm fiber)
  • 91.
    Figure 16.22b 30-nm fiber 30-nmfiber Loops Scaffold 300-nm fiber Chromatid (700 nm) Replicated chromosome (1,400 nm) Looped domains (300-nm fiber) Metaphase chromosome
  • 92.
    Figure 16.22c DNA doublehelix (2 nm in diameter)
  • 93.
  • 94.
  • 95.
  • 96.
  • 97.
    • Chromatin undergoeschanges in packing during the cell cycle • At interphase, some chromatin is organized into a 10-nm fiber, but much is compacted into a 30-nm fiber, through folding and looping • Though interphase chromosomes are not highly condensed, they still occupy specific restricted regions in the nucleus © 2011 Pearson Education, Inc.
  • 98.
  • 99.
  • 100.
  • 101.
  • 102.
    • Most chromatinis loosely packed in the nucleus during interphase and condenses prior to mitosis • Loosely packed chromatin is called euchromatin • During interphase a few regions of chromatin (centromeres and telomeres) are highly condensed into heterochromatin • Dense packing of the heterochromatin makes it difficult for the cell to express genetic information coded in these regions © 2011 Pearson Education, Inc.
  • 103.
    • Histones canundergo chemical modifications that result in changes in chromatin organization © 2011 Pearson Education, Inc.
  • 104.
    Figure 16.UN02 Sugar-phosphate backbone Nitrogenousbases Hydrogen bond G G G G C C C C A A A A T T T T
  • 105.
    Figure 16.UN03 DNA polIII synthesizes leading strand continuously Parental DNA DNA pol III starts DNA synthesis at 3′ end of primer, continues in 5′ → 3′ direction Origin of replication Helicase Primase synthesizes a short RNA primer DNA pol I replaces the RNA primer with DNA nucleotides 3′ 3′ 3′ 5′ 5′ 5′ 5′ Lagging strand synthesized in short Okazaki fragments, later joined by DNA ligase
  • 106.
  • 107.
  • 108.
  • 109.

Editor's Notes

  • #4 Figure 16.1 How was the structure of DNA determined?
  • #9 Figure 16.2 Inquiry: Can a genetic trait be transferred between different bacterial strains?
  • #12 Figure 16.3 Viruses infecting a bacterial cell.
  • #14 Figure 16.4 Inquiry: Is protein or DNA the genetic material of phage T2?
  • #15 Figure 16.4 Inquiry: Is protein or DNA the genetic material of phage T2?
  • #16 Figure 16.4 Inquiry: Is protein or DNA the genetic material of phage T2?
  • #19 Figure 16.5 The structure of a DNA strand.
  • #21 Figure 16.6 Rosalind Franklin and her X-ray diffraction photo of DNA.
  • #22 Figure 16.6 Rosalind Franklin and her X-ray diffraction photo of DNA.
  • #23 Figure 16.6 Rosalind Franklin and her X-ray diffraction photo of DNA.
  • #25 Figure 16.7 The double helix.
  • #26 Figure 16.7 The double helix.
  • #27 Figure 16.7 The double helix.
  • #30 Figure 16.UN01 In-text figure, p. 310
  • #32 Figure 16.8 Base pairing in DNA.
  • #35 Figure 16.9 A model for DNA replication: the basic concept.
  • #36 Figure 16.9 A model for DNA replication: the basic concept.
  • #37 Figure 16.9 A model for DNA replication: the basic concept.
  • #39 Figure 16.10 Three alternative models of DNA replication.
  • #42 Figure 16.11 Inquiry: Does DNA replication follow the conservative, semiconservative, or dispersive model?
  • #43 Figure 16.11 Inquiry: Does DNA replication follow the conservative, semiconservative, or dispersive model?
  • #44 Figure 16.11 Inquiry: Does DNA replication follow the conservative, semiconservative, or dispersive model?
  • #47 Figure 16.12 Origins of replication in E. coli and eukaryotes.
  • #48 Figure 16.12 Origins of replication in E. coli and eukaryotes.
  • #49 Figure 16.12 Origins of replication in E. coli and eukaryotes.
  • #50 Figure 16.12 Origins of replication in E. coli and eukaryotes.
  • #51 Figure 16.12 Origins of replication in E. coli and eukaryotes.
  • #53 Figure 16.13 Some of the proteins involved in the initiation of DNA replication.
  • #58 Figure 16.14 Incorporation of a nucleotide into a DNA strand.
  • #61 Figure 16.15 Synthesis of the leading strand during DNA replication.
  • #62 Figure 16.15 Synthesis of the leading strand during DNA replication.
  • #63 Figure 16.15 Synthesis of the leading strand during DNA replication.
  • #65 Figure 16.16 Synthesis of the lagging strand.
  • #66 Figure 16.16 Synthesis of the lagging strand.
  • #67 Figure 16.16 Synthesis of the lagging strand.
  • #68 Figure 16.16 Synthesis of the lagging strand.
  • #69 Figure 16.16 Synthesis of the lagging strand.
  • #70 Figure 16.16 Synthesis of the lagging strand.
  • #71 Figure 16.16 Synthesis of the lagging strand.
  • #72 Figure 16.16 Synthesis of the lagging strand.
  • #73 Figure 16.17 A summary of bacterial DNA replication.
  • #74 Figure 16.17 A summary of bacterial DNA replication.
  • #75 Figure 16.17 A summary of bacterial DNA replication.
  • #77 Figure 16.18 A current model of the DNA replication complex.
  • #79 Figure 16.19 Nucleotide excision repair of DNA damage.
  • #82 Figure 16.20 Shortening of the ends of linear DNA molecules.
  • #83 Figure 16.20 Shortening of the ends of linear DNA molecules.
  • #84 Figure 16.20 Shortening of the ends of linear DNA molecules.
  • #86 Figure 16.21 Telomeres.
  • #90 For the Cell Biology Video Cartoon and Stick Model of a Nucleosomal Particle, go to Animation and Video Files.
  • #91 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #92 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #93 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #94 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #95 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #96 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #97 Figure 16.22 Exploring: Chromatin Packing in a Eukaryotic Chromosome
  • #99 Figure 16.23 Impact: Painting Chromosomes
  • #100 Figure 16.23 Impact: Painting Chromosomes
  • #101 Figure 16.23 Impact: Painting Chromosomes
  • #102 Figure 16.23 Impact: Painting Chromosomes
  • #105 Figure 16.UN02 Summary figure, Concept 16.1
  • #106 Figure 16.UN03 Summary figure, Concept 16.1 2
  • #107 Figure 16.UN04 Test Your Understanding, question 10
  • #108 Figure 16.UN05 Test Your Understanding, question 12
  • #109 Figure 16.UN06 Appendix A: answer to Figure 16.17 legend question
  • #110 Figure 16.UN07 Appendix A: answer to Test Your Understanding, question 12