MDSA01H3 Lecture Notes - Lecture 8: Apoptosis, Thymine, Wear Sunscreen

27 views6 pages

greentrout185

26 Dec 2016

School

UTSC

Department

Media Studies

Course

MDSA01H3

Professor

For unlimited access to Class Notes, a Class+ subscription is required.

Document Summary

Mutated gene: can result in a protein that is either abnormal or absent totally. T and c are swaped out transition mutation- one pyrimidine/purine for another. Missence mutation- entire amino acid has changed in response to the point mutation. Protein lys to glu change to amino acid. Point mutations -3: subset of missence mutation, silent mutation no change in phenotype what so ever. That frameshift idea comes into play here. Could take the nucleotide out which changes the phenotype. Premature stop codon uaa! that"s what a (cid:374)o(cid:374) se(cid:374)se (cid:373)utatio(cid:374) is you are changing that codon and you are introducing that stop codon , Stop codon is the lack of a trna. A protein that allows the protein to be released from the ribosome. Any stop codon will have that physical release it (cid:272)a(cid:374)"t (cid:271)e used it is totally a(cid:271)(cid:374)or(cid:373)al (cid:271)e(cid:272)ause etoo (cid:373)u(cid:272)h of the polypeptide (cid:272)hai(cid:374)

Related Questions

1. The amino acid sequence of a particular polypeptide in awild-type bacterium and three single point mutant strains are shownin the following table:

Wild type= Met-Tyr-Ile-Thr-Trp-Glu-Glu-Pro-Val-Lys

Mutant 1= Met-Tyr-Ile-Thr-Trp-Asp-Glu-Pro-Val-Lys

Mutant 2= Met-Tyr-Ile-Pro-Gly-Arg-Asn-Gln

Mutant 3= Met-Tyr-His-Tyr-Leu-Gly-Gly-Thr-Ser-Lys

For each mutant indicate the type of point mutations(transition, transversion, insertion or deletion) and the codon inwhich it occurred.
B. Determine to the extent that is possible, the ribonucleotidesequence of the wild type mRNA molecule.

2. Mutations in several different genes that encode enzymes inthe pathway for the synthesis of the heme group may cause a geneticdisorder called methemoglobinemia. The symptoms of this disorderrange form mild to death in the most severe cases. The enzymecytochrome b5 reductase is one of the enzymes in this pathway. Thisenzyme is responsible for reducing the iron in the heme group tothe ferrous state so that it can bind oxygen. Kobayashi et al.reviewed several mutations in this gene. One of these mutationscauses a Ser to Pro substitution. Explain what nucleotide changeand in which position in the codon can cause this amino acidchange. Assign all possible appropriate terms to this mutation.

sapphirelizard114

1. An occurrence of a gene made larger by trinucleotide repeats is:

Allelic expansion

Nucleotide expansion

Translocation mutation

Transformation

2. a chemical that can damage and/or change DNA is called a/an:

Allele

Endonuclease

Vector

Mutagen

3. An occurrence when a section of a chromosome relocates itself to an entirely different (non-homologous) chromosome is called a/an:

Inversion mutation

Translocation mutation

Transformation mutation

Duplication mutation

4. The tandem repeat in the sequence GGGAAGGGAAGGGAAGGGAAGGGAAG is:

GGA

GGGAA

GGAAG

GGAAGGG

A disease characterized by abnormally shaped hemoglobin is called:

Cystic Fibrosis

Sickle Cell Anemia

Marfan Syndrome

Leukemia

5. A point mutation that causes a substitution of a stop codon with an amino acid and leads to the formation of a longer protein is a:

Nonsense mutation

Missense mutation

Sense mutation

Frameshift mutation

6. Addition or deletion of nucleotides in a DNA sequence is known as a:

Nonsense mutation

Missense mutation

Sense mutation

Frameshift mutation

7. The least severe type of chromosomal mutation is:

Point

Frameshift

Inversion

Translocation

8. Chemicals inserting themselves into DNA can cause a:

Missense mutation

Nonsense mutation

Sense mutation

Frameshift mutation

9. A genetic condition caused by allelic expansion is:

Familial hypercholesterolemia

Fragile X syndrome

Alkaptonuria

Galactosemia

10. Which of the following is most likely the original DNA strand if the mutated DNA strand is ATAGUUGATGUA ?

ATAGAAGATGAA

ATAGCCGATGCA

ATAGGGGATGGA

ATAGTTGATGTA

11. An unbalanced chromosomal mutation would include a/an:

duplication (insertion)

inversion

translocation

denaturation

12. Many translocation mutations are found to be involved with:

cancers

sickle cell anemia

Huntington disease

cystic fibrosis

13. A common repeat throughout the human genome that is approximately 300 bases in length is called a/an:

EcoRI repeat

Hind repeat

Exo repeat

Alu repeat

14. A balanced chromosomal mutation includes:

imprintation

denaturation

inversion

deletion

salmondinosaur263

GENETICS QUESTION: For this experiment we focused on forward genetics: First, his- mutants were identified and then complementation analysis was used in order to determine which of the 7 his genes was mutated. ( The exact data can be seen at the bottom). In this experiment we screened for his- mutants that were generated via a random mutation process resulting from errors in DNA replication or induced by EMS aka Ethyl methanesulfonate. We compared a mutagenized culture that was treated with EMS and an un-mutagenized culture that was not treated with EMS. However, both cultures went trhough an enrichment process to increase the frequency of his- mutants.

Point mutations involve the substitution of one type of base pair for another. If the substitution replaces a purine with a purine (or a pyrimidine with a pyrimidine), it is called a transition. If the substitution replaces a purine with a pyrimidine (or a pyrimidine with a purine), it is called a transversion. Many mutagenic chemicals cause this type of mutation by alkylation of a nucleotide base. The chemically altered base can then be misread during replication or repair. For example the mutagen, ethyl methanesulfonate (EMS), adds an ethyl (-CH2-CH3) group to both guanine or thymine bases causing the modified guanine to pair with thymine and the modified thymine to pair with guanine.

1. Why might one gene be more susceptible to EMS mutagenesis than another gene?

2. Why might we have expected to find a higher frequency of polar mutants (his4A^-B^-C^-) in the unmutagenized culture compared to the mutagenized culture?

Table 2. Experiment 1B class data summary (number of his^-mutants by section) Unmutagenized
Section	1	2	3	*4ABC*	4A	4B	4C	5	6	7	*Total his^-* mutants**
Tuesday	7	1	5	4	2	1	9	2	3	1	35
Wednesday	2	1	14	0	4	2	2	4	8	2	39
Total	9	2	19	4	6	3	11	6	11	3	74
% each mutant	12.1	2.7	25.7	5.4	8.1	4.1	14.9	8.1	14.9	4.1	~100%

Mutagenized
Section	1	2	3	4ABC	4A	4B	4C	5	6	7	*Total his^-* mutants**
Tuesday	2	5	4	2	6	5	5	0	4	1	34
Wednesday	9	1	15	0	9	1	2	2	9	4	52
Total	11	6	19	2	15	6	7	2	13	5	86
% each mutant	12.8	7.0	22.1	2.3	17.4	7.0	8.1	2.3	15.1	5.8	~100%

MDSA01H3 Lecture Notes - Lecture 8: Apoptosis, Thymine, Wear Sunscreen

Document Summary

Get access

Related Documents

MDSA01H3 Chapter Notes - Chapter 6: Pyrimidine Dimer, Transposase, Restriction Site

MDSA01H3 Chapter 5: Chapter 5- The Genetic Code and Trascription

BIOC15H3 Lecture Notes - Lecture 3: Phenylalanine Hydroxylase, Frameshift Mutation, Nonsense Mutation

Related Questions