Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal integrity. Each cell division causes telomeres to shorten as DNA replication cannot fully copy chromosome ends. When telomeres become too short, cells stop dividing or die. Telomerase is an enzyme that adds telomeric DNA to chromosome ends and counteracts shortening. While most somatic cells lack telomerase, its presence allows cancer cells and germ cells to avoid replicative aging. Maintaining telomere length through telomerase overexpression is a hallmark of cancer cells and targeting this process may lead to new anticancer therapies.
It describes about Structure and function of telomere, Telomerase enzyme, How does telomerase works?, Telomere replication, What happens to telomeres as we age?, Factors contribute to telomere shortening
It describes about Structure and function of telomere, Telomerase enzyme, How does telomerase works?, Telomere replication, What happens to telomeres as we age?, Factors contribute to telomere shortening
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
Chromatin is the complex combination of DNA and proteins that makes up chromosomes. It can be made visible by staining with specific techniques and stain (thus the name chromatin which literally means colored material). The major proteins involved in chromatin are histone proteins; although many other chromosomal proteins have prominent roles too. The functions of chromatin is to package DNA into smaller volume to fit in the cell, to strengthen the DNA to allow mitosis and meiosis and to serve as a mechanism to control gene expression and DNA replication.
Telomere, Functions & Role in Aging & CancerZohaib HUSSAIN
Why senescence occurs in eukaryotic organisms?
The major function of telomere is to cap the ends of chromosomes and protect the chromosomes from RED mechanism. As cells divide, telomeres continuously shorten with each successive cell division. Telomerase provides the necessary enzymatic activity to restore and maintain the telomere length. The vast majority of tumour's activate telomerase , and only few maintain telomeres by ALT mechanism relying on recombination. Telomere and telomerase are the attractive targets for anti-cancer therapeutics
Sanger sequencing is one of the DNA sequencing methods used to identify and determine the sequence (Nucleotide) of DNA .This is an enzymatic method of sequencing developed by Fred Sanger.
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
Chromatin is the complex combination of DNA and proteins that makes up chromosomes. It can be made visible by staining with specific techniques and stain (thus the name chromatin which literally means colored material). The major proteins involved in chromatin are histone proteins; although many other chromosomal proteins have prominent roles too. The functions of chromatin is to package DNA into smaller volume to fit in the cell, to strengthen the DNA to allow mitosis and meiosis and to serve as a mechanism to control gene expression and DNA replication.
Telomere, Functions & Role in Aging & CancerZohaib HUSSAIN
Why senescence occurs in eukaryotic organisms?
The major function of telomere is to cap the ends of chromosomes and protect the chromosomes from RED mechanism. As cells divide, telomeres continuously shorten with each successive cell division. Telomerase provides the necessary enzymatic activity to restore and maintain the telomere length. The vast majority of tumour's activate telomerase , and only few maintain telomeres by ALT mechanism relying on recombination. Telomere and telomerase are the attractive targets for anti-cancer therapeutics
Sanger sequencing is one of the DNA sequencing methods used to identify and determine the sequence (Nucleotide) of DNA .This is an enzymatic method of sequencing developed by Fred Sanger.
Telomere Length as a Predictor for Longevity and Specific MortalityDavid Rehkopf
An overview of research on telomere length and mortality, including a consideration of observational data and genetic instrumental variable analysis, as well as a primer on practical technical issues of doing studies on telomere length to understand biological aging.
Cambridge Pre-U Biology - 1.3 DNA Replicationmrexham
This is part of the PowerPoint that covers section 1.2 in the Cambridge Pre-U Biology course. The full PowerPoint covers the following topics: Prokaryotic cell structure, asexual reproduction, introduction to antibiotics, bacterial pathogens.
It can be purchased from here: https://sellfy.com/p/nktT/#
Subject - Management
Unit 1 - introduction to marketing management
Content- Marketing, Marketing Management, Markets, What can Marketed? etc.
Marketing management is the art and science of choosing target markets and getting, keeping, and growing customers through creating, delivering, and communicating superior customer value.
Introduction to Women's and Gender Studies Lectureamyhudock
I took many of the slides from the powerpoint presentation called Intro to Gender 2000, but I adapted the slideshow for my own use. I also used the template provided by the slideshow. I provide a link to the original at the end of the slideshow.
Telomere is the end part of a chromosome.its length is maintained by na enzyme called telomerase.if telomerase is lacking,many genetic diseases may result( like progeria)
This presentation describes the structure and function of telomeres ,their role in various disease.The structure and function of telomerase is also described ,together with its possible role in therapy .
Dr. Al Sears explains the Nobel Prize winning breakthrough telomere technology. This opened the way for Harvard researcher, Dr. Ronal DePinho to find a way to activate telomerase. Telomerase is the enzyme that signals your telomeres to grow longer, unfortunately, it shuts down while you are still in your mother's womb.
Once Nobel Prize winning research identified that telomeres are the protective tips at each end of the strands of your DNA, and as your cells replicate, gradully your telomeres grow shorter. They are the "aging-clocks" inside your DNA.
Once Dr. DePinho found a way to reactivate the telomerase enzyme, he turned old mice into young mice again.
Not long after, scientists discovered ways to do this in humans as well, and today, the discovery of the telomere and telomerase are the most important anti-aging breakthrough of our time.
Telomere is the end part of the eukaryotic chromosomes and they need special way to replicate theirselves because of regular DNA replication can’t replicate the ends of eukaryotic chromosomes.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
Slide 1: Title Slide
Extrachromosomal Inheritance
Slide 2: Introduction to Extrachromosomal Inheritance
Definition: Extrachromosomal inheritance refers to the transmission of genetic material that is not found within the nucleus.
Key Components: Involves genes located in mitochondria, chloroplasts, and plasmids.
Slide 3: Mitochondrial Inheritance
Mitochondria: Organelles responsible for energy production.
Mitochondrial DNA (mtDNA): Circular DNA molecule found in mitochondria.
Inheritance Pattern: Maternally inherited, meaning it is passed from mothers to all their offspring.
Diseases: Examples include Leber’s hereditary optic neuropathy (LHON) and mitochondrial myopathy.
Slide 4: Chloroplast Inheritance
Chloroplasts: Organelles responsible for photosynthesis in plants.
Chloroplast DNA (cpDNA): Circular DNA molecule found in chloroplasts.
Inheritance Pattern: Often maternally inherited in most plants, but can vary in some species.
Examples: Variegation in plants, where leaf color patterns are determined by chloroplast DNA.
Slide 5: Plasmid Inheritance
Plasmids: Small, circular DNA molecules found in bacteria and some eukaryotes.
Features: Can carry antibiotic resistance genes and can be transferred between cells through processes like conjugation.
Significance: Important in biotechnology for gene cloning and genetic engineering.
Slide 6: Mechanisms of Extrachromosomal Inheritance
Non-Mendelian Patterns: Do not follow Mendel’s laws of inheritance.
Cytoplasmic Segregation: During cell division, organelles like mitochondria and chloroplasts are randomly distributed to daughter cells.
Heteroplasmy: Presence of more than one type of organellar genome within a cell, leading to variation in expression.
Slide 7: Examples of Extrachromosomal Inheritance
Four O’clock Plant (Mirabilis jalapa): Shows variegated leaves due to different cpDNA in leaf cells.
Petite Mutants in Yeast: Result from mutations in mitochondrial DNA affecting respiration.
Slide 8: Importance of Extrachromosomal Inheritance
Evolution: Provides insight into the evolution of eukaryotic cells.
Medicine: Understanding mitochondrial inheritance helps in diagnosing and treating mitochondrial diseases.
Agriculture: Chloroplast inheritance can be used in plant breeding and genetic modification.
Slide 9: Recent Research and Advances
Gene Editing: Techniques like CRISPR-Cas9 are being used to edit mitochondrial and chloroplast DNA.
Therapies: Development of mitochondrial replacement therapy (MRT) for preventing mitochondrial diseases.
Slide 10: Conclusion
Summary: Extrachromosomal inheritance involves the transmission of genetic material outside the nucleus and plays a crucial role in genetics, medicine, and biotechnology.
Future Directions: Continued research and technological advancements hold promise for new treatments and applications.
Slide 11: Questions and Discussion
Invite Audience: Open the floor for any questions or further discussion on the topic.
2. CONTENTS
• Introduction of telomere
• Structure
• Telomere as a multi protein complex
• Functions
• Telomere and aging
• Link between telomere and telomerase
• Telomere biology and cancer
3. INTRODUCTION
• A telomere is a region of repetitive nucleotide
sequences at each end of a chromosome.
• Blackburn, Carol Greider and Jack Szostak
were awarded the 2009 Nobel prize in
physiology and medicine for the discovery of
telomere and telomerase.
4. INTRODUCTION
• Unique structures at the end of chromosomes are
necessary for chromosomal integrity and overall
genomic stability called as telomeres which
protect our genetic data, make it possible for cells
to divide, and hold some secrets to how we grow
old and get cancer.
• An entire chromosome has about 150 million base
pairs. Each time a cell divides, an average person
loses 30 to 200 base pairs from the ends of that
cell's telomeres
6. STRUCTURE…..
• Telomeres are comprised of repeat sequences
and bound by multiple telomeric interacting
proteins. In mammalian cells, telomere DNA
contains double-stranded tandem repeats of
TTAGGG followed by terminal 3′ G-rich single-
stranded overhangs. Telomere DNA is thought
to adopt the T-loop structure, where the
telomere end folds back on itself and the 3′ G
strand overhang invades into the double-
stranded DNA (the so-called D-loop).
7. Telomere : a multi protein complex
• Mammalian telomeres have a SIX PROTEIN complex called
“SHELTERIN”.
• TRF1 and TRF2 bind to the TTAGGG sequences in the double strand
telomeric DNA.
• POT1 binds to the sequences in single strand form
• TIN2 and TPP1 proteins keep TRF1, TRF2 and POT1 together.
• This six protein complex, SHELTERIN prevents the activation of the DNA
damage response.
• SHELTERIN is required for the recruitment of telomerase.
9. FUNCTIONS
• They protect the chromosomes.
• They separate one chromosome from another
in the DNA sequence.
• Without telomeres, the ends of the
chromosomes would be "repaired", leading to
chromosome fusion and massive genomic
instability.
10. FUNCTION CONT….
• Telomeres are also thought to be the "clock"
that regulates how many times an individual
cell can divide. Telemetric sequences shorten
each time the DNA replicates.
12. A) The telomeres are seen as the
bright red signals on the
chromosome ends.
B) Fusions between the
chromosomes are indicated by
the arrows, no telometric DNA is
observed at these points.
13. Telomeres and aging
• It has been proposed that telomere shortening
may be a molecular clock mechanism that counts
the number of times a cell has divided and when
telomeres are short, cellular senescence (growth
arrest) occurs.
• It is believed that shortened telomeres in mitotic
(dividing) cells may be responsible for some of
the changes we associate with normal aging.
14. Cells normally can divide only about 50 to 70
times, with telomeres getting progressively
shorter until the cells become senescent, die or
sustain genetic damage that can cause cancer.
Example:
In human blood cells, the length of telomeres
ranges from 8,000 base pairs at birth to 3,000
base pairs as people age and as low as 1,500 in
elderly people.
Telomeres do not shorten with age in tissues
such as heart muscle in which cells do not
continually divide.
15. People who are older have
chromosomes that have replicated
more times.
17. Why do telomeres get shorter each
time a cell divides?
• While replicating DNA, the eukaryotic DNA
replicating enzymes, cannot replicate the
sequences present at the end of chromosomes.
Hence these sequences and the information
they carry may get lost.
• They cap the end sequences and themselves
get lost in the process of DNA replication.
• In 1972, James Watson called this as End-
replication problem.
18. Since the DNA structure can be rebuilt on both
parent strands, two identical DNA helices are
produced, each containing one original parent
strand and one newly synthesized strand, called a
complementary strand.
Due to the nature of the mechanism via which
DNA is replicated, one strand of the DNA is left
with an incompletely replicated end. Without
specialized means of maintaining chromosomes,
this causes chromosome ends to shrink with each
successive cell division.
20. WHAT NEXT?
• Dr. Jerry Shay and his colleagues (The
University of Texas Southwestern Medical
Center at Dallas ) found that cellular
aging can be bypassed or put on hold by
the introduction of the catalytic
component of telomerase.
21. TELOMERASE
• Telomerase (TEE-LÓM-ER-ACE) is a
ribonucleoprotein enzyme complex (a cellular
reverse transcriptase) that has been referred
to as a cellular immortalizing enzyme.
• It stabilizes telomere length by adding
hexametric (TTAGGG) repeats onto the
telomeric ends of the chromosomes, thus
compensating for the erosion of telomeres
that occurs in its absence
22. HOW DOES TELOMERASE WORKS?
• Telomerase works by adding back telomeric
DNA to the ends of chromosomes, thus
compensating for the loss of telomeres that
normally occurs as cells divide.
• Most normal cells do not have this enzyme
and thus they lose telomeres with each
division.
23. HOW DOES TELOMERASE WORKS?
• In humans, telomerase is active in germ cells,
in vitro immortalized cells, the vast majority of
cancer cells and, possibly, in some stem cells.
• High telomerase activity exists in germ cells,
stem cells, epidermal skin cells, follicular hair
cells, and cancer cells.
24. HOW DOES TELOMERASE WORKS?
• Some cells are immortal because their
telomerase is switched on
• Examples of immortal cells: blood cells
and cancer cells
• Cancer cells do not age because they
produce telomerase, which keeps the
telomere intact.
25. Telomere and CANCER
• Telomeres were first discovered in cancer cells
because, cancer cells are saturated with an
enzyme called telomerase.
• Telomerase is the key enzyme for human cells to
accquire immortality.
• As a cell begins to cancerous, it divides more
often and its telomere becomes very short. If its
telomeres get too short, the cell may die, whereas
normal cell is devoid of telomerase activity.
26. Telomere and CANCER
• It can escape this fate by becoming cancerous cell by
activating telomerase (or) ALT pathway is activated,
resulting in abnormal
telomere lengthening & proliferative growth
• Telomerase is over expressed in many cancers cells.
• When cells lose the function of P53 pathway, they can
no longer arrest cells in G1 an important point in cell
cycle for repairing DNA damage response. Cells
without P53 are able to divide with deprotected
telomeres, which cause genomic instability a common
feature of malignant cells.
27.
28.
29. CONCLUSION…
• Measuring telomerase may be a new way to
detect cancer.
• If scientists can learn how to stop telomerase, they
might be able to fight with cancer by making
cancer cells age and die.
• Some of the drugs are showed positive results by
inhibiting telomerase and associated proteins and
finding the way to shortening of telomere which
results in cell death/apoptosis.
• Most of anti-telomerase drugs are still in Clinical
phases I and II.
30. REFRENCES (1 OF 2)
• Role of telomere and telomerase — Elizabeth
Blackburn.
• Telomeres—structure, function, and regulation—
Weisi Lua, YiZhangb, DanLiub,
ZhouSongyanga,b,c,n, MaWanb,
• Telomeres and telomerase as targets for
anticancer drug development—Ken André
Olaussen a, Karine Dubrana a, Julien Domonta,
Jean-Philippe Spano b,
31. REFRENCES (2 OF 2)
• Geron Symposium No. 3 “Telomerase and
Telomere Dynamics in Cancer and Aging”
(www.geron.com/)
• “Mouse model demonstrates role of
telomeres and telomerase in aging, cancer
and lifespan” (http://www.arclab.org/ March
4, 1999 )
