SepBCTF4 is required for the formation of DNA-damage-induced UvsCRAD51 foci in Aspergillus nidulans.

نویسندگان

  • Scott E Gygax
  • Camile P Semighini
  • Gustavo H Goldman
  • Steven D Harris
چکیده

SepB is an essential, conserved protein required for chromosomal DNA metabolism in Aspergillus nidulans. Homologs of SepB include yeast Ctf4p and human hAnd-1. Molecular and bioinformatic characterization of these proteins suggests that they act as molecular scaffolds. Furthermore, recent observations implicate the yeast family members in lagging-strand replication and the establishment of sister-chromatid cohesion. Here, we demonstrate that SepB functions in the A. nidulans DNA damage response. In particular, analysis of double mutants reveals that SepB is a member of the UvsC(RAD51) epistasis group. In accord with this prediction, we show that UvsC(RAD51) forms DNA-damage-induced nuclear foci in a manner that requires SepB function. We also provide evidence that implicates SepB in sister-chromatid cohesion, thereby suggesting that cohesion may play a role in regulating the localization and/or assembly of UvsC(RAD51) complexes.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The Aspergillus nidulans uvsB gene encodes an ATM-related kinase required for multiple facets of the DNA damage response.

In Aspergillus nidulans, uvsB and uvsD belong to the same epistasis group of DNA repair mutants. Recent observations suggest that these genes are likely to control cell cycle checkpoint responses to DNA damage and incomplete replication. Consistent with this notion, we show here that UVSB is a member of the conserved family of ATM-related kinases. Phenotypic characterization of uvsB mutants sho...

متن کامل

Aspergillus nidulans uvsBATR and scaANBS1 genes show genetic interactions during recovery from replication stress and DNA damage.

The ATM/ATR kinases and the Mre11 (Mre11-Rad50-Nbs1) protein complex are central players in the cellular DNA damage response. Here we characterize possible interactions between Aspergillus nidulans uvsB(ATR) and the Mre11 complex (scaA(NBS1)). We demonstrate that there is an epistatic relationship between uvsB(ATR), the homolog of the ATR/MEC1 gene, and scaA(NBS1), the homolog of the NBS1/XRS2 ...

متن کامل

Regulation of septum formation in Aspergillus nidulans by a DNA damage checkpoint pathway.

In Aspergillus nidulans, germinating conidia undergo multiple rounds of nuclear division before the formation of the first septum. Previous characterization of temperature-sensitive sepB and sepJ mutations showed that although they block septation, they also cause moderate defects in chromosomal DNA metabolism. Results presented here demonstrate that a variety of other perturbations of chromoso...

متن کامل

Regulation of hyphal morphogenesis and the DNA damage response by the Aspergillus nidulans ATM homolog AtmA.

Ataxia telangiectasia (A-T) is an inherited disorder characterized by progressive loss of motor function and susceptibility to cancer. The most prominent clinical feature observed in A-T patients is the degeneration of Purkinje motor neurons. Numerous studies have emphasized the role of the affected gene product, ATM, in the regulation of the DNA damage response. However, in Purkinje cells, the...

متن کامل

Genetic interactions of the Aspergillus nidulans atmAATM homolog with different components of the DNA damage response pathway.

Ataxia telangiectasia mutated (ATM) is a phosphatidyl-3-kinase-related protein kinase that functions as a central regulator of the DNA damage response in eukaryotic cells. In humans, mutations in ATM cause the devastating neurodegenerative disease ataxia telangiectasia. Previously, we characterized the homolog of ATM (AtmA) in the filamentous fungus Aspergillus nidulans. In addition to its expe...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Genetics

دوره 169 3  شماره 

صفحات  -

تاریخ انتشار 2005