Deger, N., Cao, X., Selby, C.P., Gulec, S., Kawara, H., Dewey, E.B., Wang, L., Yang, Y., Archibald, S., Selcuk, B., Adebali, O., Sekelsky, J., Sancar, A., Liu, Z. (2022). CSB-independent, XPC-dependent transcription-coupled repair in Drosophila.  Proc. Natl. Acad. Sci. U.S.A. 119(9): e2123163119.

FBrf0252784

Research paper

Drosophila melanogaster has been extensively used as a model system to study ionizing radiation and chemical-induced mutagenesis, double-strand break repair, and recombination. However, there are only limited studies on nucleotide excision repair in this important model organism. An early study reported that Drosophila lacks the transcription-coupled repair (TCR) form of nucleotide excision repair. This conclusion was seemingly supported by the Drosophila genome sequencing project, which revealed that Drosophila lacks a homolog to CSB, which is known to be required for TCR in mammals and yeasts. However, by using excision repair sequencing (XR-seq) genome-wide repair mapping technology, we recently found that the Drosophila S2 cell line performs TCR comparable to human cells. Here, we have extended this work to Drosophila at all its developmental stages. We find TCR takes place throughout the life cycle of the organism. Moreover, we find that in contrast to humans and other multicellular organisms previously studied, the XPC repair factor is required for both global and transcription-coupled repair in Drosophila.

PMC8892495 (PMC) (EuropePMC)