Publications by authors named "W Wiegant"
Article Synopsis
- During DNA repair, some types of damage cause breaks in the DNA, and a special group called the Fanconi anemia (FA) core complex helps fix these breaks.
- Researchers found that two members of this complex, FANCL and Ube2T, play an important role in fixing DNA breaks even when they aren't caused by interstrand crosslinks (ICLs).
- The study showed that FANCL helps gather other repair proteins at the break sites, making it easier for the cell to fix the DNA properly.
Article Synopsis
- Homologous Recombination (HR) is a precise mechanism that repairs DNA Double-Strand Breaks (DSBs), which can occur due to various damaging factors like radiation or chemicals.
- The study identified members of the Fanconi anemia (FA) core complex, specifically FANCL and Ube2T, as key players in promoting HR at DSBs, even independent of interstrand crosslinks (ICLs).
- The findings also highlight that FANCL's activity is crucial for recruiting the nuclease CtIP to DSB sites, which is necessary for effective HR, suggesting a dual role for the FA complex in DNA repair.
Nucleosome assembly requires the coordinated deposition of histone complexes H3-H4 and H2A-H2B to form a histone octamer on DNA. In the current paradigm, specific histone chaperones guide the deposition of first H3-H4 and then H2A-H2B. Here, we show that the acidic domain of DNA repair factor APLF (APLF) can assemble the histone octamer in a single step and deposit it on DNA to form nucleosomes.
View Article and Find Full Text PDFUnlabelled: Heterozygous carriers of germline loss-of-function variants in the tumor suppressor gene checkpoint kinase 2 (CHEK2) are at an increased risk for developing breast and other cancers. While truncating variants in CHEK2 are known to be pathogenic, the interpretation of missense variants of uncertain significance (VUS) is challenging. Consequently, many VUS remain unclassified both functionally and clinically.
View Article and Find Full Text PDFDNA double-strand breaks (DSBs) are among the most deleterious types of DNA damage as they can lead to mutations and chromosomal rearrangements, which underlie cancer development. Classical non-homologous end-joining (cNHEJ) is the dominant pathway for DSB repair in human cells, involving the DNA-binding proteins XRCC6 (Ku70) and XRCC5 (Ku80). Other DNA-binding proteins such as Zinc Finger (ZnF) domain-containing proteins have also been implicated in DNA repair, but their role in cNHEJ remained elusive.
View Article and Find Full Text PDF