Abstract
The DNA replication process represents a source of DNA stress that causes potentially spontaneous genome damage. This effect might be strengthened by mutations in crucial replication factors, requiring the activation of DNA damage checkpoints to enable DNA repair before anaphase onset. Here, we demonstrate that depletion of the evolutionarily conserved minichromosome maintenance helicase-binding protein ETG1 of Arabidopsis thaliana resulted in a stringent late G2 cell cycle arrest. This arrest correlated with a partial loss of sister chromatid cohesion. The lack-of-cohesion phenotype was intensified in plants without functional CTF18, a replication fork factor needed for cohesion establishment. The synergistic effect of the etg1 and ctf18 mutants on sister chromatid cohesion strengthened the impact on plant growth of the replication stress caused by ETG1 deficiency because of inefficient DNA repair. We conclude that the ETG1 replication factor is required for efficient cohesion and that cohesion establishment is essential for proper development of plants suffering from endogenous DNA stress. Cohesion defects observed upon knockdown of its human counterpart suggest an equally important developmental role for the orthologous mammalian ETG1 protein.
Highlights
For one single cell to generate two cells, numerous events must be coordinated, in particular, faithful DNA replication and partitioning of the sister chromatids to each of the daughter cells
It is of utmost importance that the damaged DNA is repaired before cells proceed through mitosis, because the genome holds all the information required for correct development
We identified the Arabidopsis thaliana E2F TARGET GENE 1 (ETG1) protein as a novel evolutionarily conserved replication factor that is needed for maintaining the sister chromatids physically aligned
Summary
For one single cell to generate two cells, numerous events must be coordinated, in particular, faithful DNA replication and partitioning of the sister chromatids to each of the daughter cells. DNA damage and replication errors might originate from DNA stress provoked by either exogenous (such as cirradiation and UV-B light) or endogenous (such as metabolic byproducts) sources The latter include the replication process itself that necessitates the cooperation of many different proteins in a highly complex manner. Errors arisen during replication are preferentially repaired through homologous recombination between the replicated sister chromatids that lay in close proximity thanks to cohesion. This sister chromatid cohesion is mediated by cohesin that consists of four subunits in budding yeast (Saccharomyces cerevisiae): two structural maintenance of chromosome (SMC) proteins, designated SMC1 and SMC3, and two non-SMC subunits, designated SCC1 ( known as Mcd1/Rad21) and SCC3 [1,2,3,4,5]. Cohesin forms a tripartite ring in which the open-V structure of the SMC heterodimer is closed by the simultaneous binding of the N- and C-terminal regions of SCC1 to the head domains of SMC3 and SMC1, respectively [8]
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