Note for: Effects of double-strand break repair proteins on vertebrate telomere structure

Note for: Effects of double-strand break repair proteins on vertebrate telomere structure

(Nucleic Acids Res. 2002 Jul 1; 30(13): 2862–2870)

Phenotype between mouse and DT40 on the telomere --> Ku(-/-) different

At the very end;

the authors conclude that "significant species-specific differences" in telomeric fn of DSB repair proteins.

Telomeres are stable structure and invisible to DNA repair machinery, or else there will be the fusion of chromosome.

Telomeres --> appeared as DNA-protein cpx. --> selective for telomerase to access but not end-DNA processing enzymes.

There is the report showing that if there is no telomerase, telomere is maintained by recombination-based pw.

Evidents showed that when KO genes in DNA repair group --> there is the defects in telomere structure;

1. telomere shortening

2. alterations to terminal DNA structure

3. end-to-end fusions

Gap;

They don't know how DNA repair protein involved with the telomere.

Purpose of this study--> want to learn more on telomere biology in vertebrate cells, thus, they use DT40+theirs KO in specific HR/NHEJ and observe the phenotypes on telomere.

the authors claim that telomere's structure in chicken and in mammalian is similar. Not only the structure that they mentioned, they also informed that protein set involving in telomere proteins; TRF1, TRF2, Pot1, RAP1 and tankyrase --> conserved between chickens and humans.

List of DNA repair proteins (DSB) that they focus;

1. Ku70

2. DNA-PK

3. Mre-11

4. Rad51

5. Rad52

6. Rad54

7. XRCC2

8. XRCC3

--

Phenotypes on telomere that they want to look

1. G-overhang structure

2. Telomere length

They mentioned that culture (DT40-Ku70-/-) that long-term cultured --> caused telomere length differentiation -->so they sort the DT40-Ku70-/- cell;

1. short telomere (3kb)

2. long telomere (5-6kb)

The author raised the point on the backcross when using mouse that can generate the variability, but if compare to the DT40, the resulted phenotype comes from the participant gene.

Most of the result is negative, only Rad51 has very very little effect on the telomere. So the authors conclude that DSB repair protein (part not all) participate in telomere but it has different role between DSB and telomere....