Publication details

Factors of genome stability in moss Physcomitrella patens



Year of publication 2018
Type Conference abstract
Description Genome stability is essential for the proper cellular function and is maintained by various DNA repair systems. Without adequate protection, the ends of linear chromosomes can be recognized as double-strand breaks (DSB). Telomeres, special terminal nucleoprotein structures, help to distinguish natural chromosome ends from DSB and thus prevent their unwanted repair and chromosomal fusions. Paradoxically, many of DNA repair factors were localized at telomeres forming functional complexes. In contrast to most higher eukaryotes, including flowering plants, preferentially using nonhomologous end-joining (NHEJ) pathways of DSB repair, the moss Physcomitrella patens is more proficient in homology-dependent repair (HR). Previous results showed the connection of DNA repair preference with the divergent impact of mutations in DNA repair factors, including the absence of telomere phenotype in P. patens mutants in NHEJ factors, in contrast to Arabidopsis. Here we focus on RAD51 protein which is involved in HR, catalyzing the key strand-invasion step in most eukaryotes. We investigate whether its loss of function in an organism with HR preference affects telomere homeostasis. Another factor affecting genome stability is replication stress induced by the G-rich telomeric repeats forming stable G-quadruplex structures. The best-characterized helicase solving this problem is RTEL1 (Regulator of Telomere Elongation 1). Preliminary results of telomere length analysis showed no changes in telomere lengths in the pprad51ab mutant, while pprtel1 mutant displays enormous telomere shortening. This is consistent with the predicted role of RTEL1 in T-loop resolution facilitating telomere replication. Because of the frequent linkage of telomeric phenotype and change in copy-number of ribosomal genes, we also tested if depletion of RAD51A/B and RTEL1 genes affects 18S rDNA copy number in P. patens. Interestingly, results show significant loss of 18S rDNA copies in both mutants.

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