In today’s new issue of JCB, two papers describe how cells generate and then dismantle reversed replication forks, DNA structures that help cells overcome impediments to DNA replication without introducing chromosome breaks. Zellweger et al. report that the homologous recombination protein RAD51 helps generate reversed forks in response to numerous genotoxic insults, while Thangavel et al. reveal that the nuclease DNA2 and the helicase WRN help resolve these structures so that cells can safely resume DNA replication. Both papers are summarized in this week’s In Focus here.
Xiong et al. reveal that a protein that helps mouse embryonic stem cells retain their identity also spurs the cells to repair DNA damage. The stemness factor Sall4, which suppresses the differentiation of embryonic stem cells, also helps to recruit and activate the DNA repair protein ATM at double strand breaks, potentially explaining why embryonic stem cells repair DNA damage more efficiently than other cell types. More here.
Albrecht et al. demonstrate that phosphorylation and methylation of the desmosomal protein desmoplakin is required for the proper assembly of intercellular junctions. As described here, the authors show that a mutation linked to arrhythmogenic cardiomyopathy abolishes one of desmoplakin’s methylation sites, reducing the protein’s phosphorylation by the kinase GSK3 and delaying the formation of intercellular adhesions.
Elsewhere, Lee et al. describe how ribonucleoprotein assemblies control symmetry breaking and polarized fungal cell growth, and Ioannou et al. reveal how the small GTPase Rab13 promotes cell protrusion and cancer cell metastasis. You can hear from the authors of both studies in this month’s biobytes podcast. Listen below or subscribe in iTunes.
That’s all for now, but you can see all of the papers from our latest issue by visiting the table of contents page here.
Cover image of cells expressing a mutant version of desmoplakin (green) © 2015 Albrecht et al.