This document discusses initiation codons, termination codons, mutation codons, and the genetic code. It begins by explaining that initiation codons (usually AUG) code for methionine and signal the start of protein translation. Termination codons (UAG, UAA, UGA) do not code for amino acids and cause the release of the polypeptide chain. Point mutations include substitutions, insertions, deletions, and frameshifts that can alter the amino acid sequence. The genetic code is the set of rules by which nucleic acid sequences are translated into proteins.

1. INITIATION AND TERMINATION
CODONS , MUTATION AND GENETIC
CODE

2. CONTENTS
Initiation codon
Termination codon
Mutation codon
Genetic code

3. INITIATION CODON
• The start codon is the first codon of a messenger RNA transcript
translated by a ribosome.
• The start codon always codes for methionine in eukaryotes and
a modified met ( f Met ) in prokaryotes.
• The most common start codon is AUG.
• The start codon is often preceded by a 5' untranslated region
( 5' UTR ) .

4. • The discovery of a t RNA specific for N – formylmethionine ( t RNAFmet )
initially suggested that it would recognize a codon different from the
AUG methionine codon.
• But as a elucidation of the t RNAF met sequence revealed that its
anticodon 3' – UAC – 5' was identical to that of the RNAM met.
• Both f Met and Met must therefore be directly coded by AUG.
• Discrimination between the two forms occurs through their differential
binding by protein synthesis factors.

5. • Only fmet – t RNAF met can bind to the initiation factor IF2 to
form the 30 S initiation complex ; and only Met – t RNA M met is
able to bind to the elongation factor EF – Tu during polypeptide
chain elongation.
• A further complication is the realisation, coming first from in
vitro studies and later from m RNA sequences, that f Met – t RNA
F met can bind to and initiate synthesis at GUG as well as AUG
codons.
• GUG is used as an initiator codon only about one – thirteenth as
frequently as AUG initiators in E.coli.

6. • Normally, GUG is a valine codon and its recognition by tRNA F met
would require an unusual sort of wobble in the codon – anticodon
interaction.
• The ambiguity is at the first (5') as opposed to the third (3') position
of the codon and would therefore involve the 3' base of the
anticodon.
• A possible explanation for the unexpected ability of the initiator t
RNA to engage in first – position wobble lies in the t RNA F met
sequence.

7. • The nucleotide adjacent to the 3' end of the anticodon is an
unmodified adenine, not the bulky alkylated derivative found in
virtually all other t RNAS.
• In fact, UUG and CUG codons also specify initiation, although
even more rarely than GUG.
• Thus, the unique wobble capability of the third (3') position of
the t RNAFmet anticodon seems to extend to all possible
partners.

8. TERMINATION CODONS
• There are 3 stop codons in the genetic code – UAG, UAA, and UGA.
• These codons are also known as nonsense codons or termination
codons as they do not code for an amino acid.
• The three stop codons have been named as amber [ UAG ] , opal or
umber [ UGA ] and ochre [ UAA].
• Amber or UAG was discovered by Charles Steinberg and Richard
Epstein and they named it amber after the German meaning of the
last name of their friend Harris Bernstein.

9. • The remaining two STOP codons were then named " Ocher " and
" opal " so as to maintain the " colour names " theme.
• During protein synthesis, STOP codons cause the release of the
new polypeptide chain from the ribosome.
• This occurs because there are no t RNAS with anticodons
complementary to the STOP codons.
• Two release factors, RF1 and RF2, have been identified, each of
which recognizes two codons.
• One is specific for USA and UAG and the other for UAA and UGA.

10. • The use of proteins to read the stop signals emphasizes the fact
that not only polynucleotide can specifically interact with other
polynucleotides.
• The specific hydrogen – bond – forming groups of the bases can
also be recognized by proteins containing specific constellations
of amino acids that have groups prone to hydrogen bonding.
• The presence of more than one stop codon may be a precaution
against the rare case in which the first codon fails, but why this
device is used only occasionally is unclear.

11. MUTATION CODON

12. Point Mutation

13. • A point mutation is specifically when only one nucleotide base is
changed in some way, although multiple point mutations can
occur in one strand of DNA or RNA.
• Point mutations are sometimes caused by mutations that
spontaneously occur during DNA replication.
• The rate of mutations may also increase when a cell is exposed
to mutagenes, which are environmental factors that can change
an organisms DNA.
• Some mutages are X – rays , UV rays , extreme heat , or certain
chemicals like benzene.

14.  Substitution : –
• A substitution mutation occurs when one base pair is
substituted for another.
• For example, this would occur when one nucleotide
containing cytosine is accidentally substituted for one
containing guanine.
• There are three types of substitution mutations : –
a ) Silent Mutation
b ) Missene Mutation
c ) Nonsense Mutation

15. a ) Silent Mutation : –
• In a silent mutations, a nucleotide is substituted but the same
amino acid is produced anyway.
• This can occur because multiple codons can code for the same
amino acid.
• For example, AAG and AAA both code for lysine , so if the G is
changed to an A, the same amino acid will form and the Protein
will not be affected.

16. b ) Missense Mutation : –
• This type of Mutation is a change in one DNA base paire that
results in the substitution of one amino acid for another in the
Protein made by a gene.
c ) Nonsense Mutation : –
• A nonsense mutation is also a change in one DNA basepair.
• Instead of substituting one amino acid for another, however,
the altered DNA sequence prematurely signals the cell to stop
building a protein.
• This type of mutation results in a shorted protein that may
function improperly or not at all.

18. Frameshift Mutation
• This type of mutation occurs when the addition or loss of DNA
bases changes a gene's reading frame.
• A reading frame consists of groups of 3 bases that each code for
one amino acid.
• A frameshift mutation shifts the grouping of these bases and
changes the code for amino acids.
• The resulting protein is usually non functional.
• Insertion, deletion and duplications can all be frameshift
mutations.

19. a ) Insertion : –
• An insertion changes the number of DNA based in a gene by
adding a piece of DNA.
• As a result, the protein made by the gene may not function
properly.
b ) Deletion : –
• A deletion changes the number of DNA bases by removing a
piece of DNA.
• Small deletions may remove one or a few base pairs within a
gene, while large deletions can remove an entire gene or
several neighbouring genes.

20. • The deleted DNA may alter the function of the resulting
proteins.
c ) Duplication : –
• A duplication consists of a piece of DNA abnormally copied one
or more times.
• This type of mutation may alter the function of the resulting
protein.

22. GENETIC CODE
• Translation is the process of conservation of nucleic acid
information into amino acids.
• This genetic information is encrypted in the form of code called
genetic code or codon.
• The genetic code is a set of information encoded in the sequence
of nucleic acids that does the coding for proteins to be
synthesized.
• Any change in genetic codes might lead to mutation.

23. • Let us understand mutation in terms of genetic codes.
• Genes are the functional units of heredity of organisms.
• It is mainly responsible for the structure and functional changes
and for the variation in organisms which could be good or bad.
• Even a minute change in the DNA sequence could alter the amino
acids to be produced and proteins to be synthesized.
• The genetic code is a dictionary that corresponds with the
sequence of nucleotides and sequence of the amino acids.

24. REFERENCES
• Molecular biology by : – Veer Bala Rastogi
• Molecular Biology Of The Gene by : —
Watson, Hopkins, Roberts, Steitz, Weiner
• Genetics by : – P. S. Verma & V. K. Agarwal
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