Alexander Duckworth

Abstract Replication restart pathways reinitiate DNA replication processes following their premature termination. In Escherichia coli, this essential process begins with regulated assembly of the preprimosome complex, comprising the PriA, PriB, and DnaT proteins, onto an abandoned replication fork. Here, we present two distinct preprimosome structures. One represents an intermediate stage in preprimosome assembly with a single DnaT C-terminal domain (DnaTCTD) bound to PriA/PriB/DNA.

Highlights • ATF6 and IRE1α deletion in NOD β cells before insulitis triggers early senescence • p21-mediated secretome induces the recruitment of M2 macrophages to the islets • ATF6 and IRE1α deficiency reduces terminal β cell senescence and diabetes incidence • Early senescence signature is conserved in residual β cells of T1D patients Summary During the progression of type 1 diabetes (T1D), β cells are exposed to significant stress and, therefore, require adaptive responses to survive.

Abstract Bacterial replisomes often dissociate from replication forks before chromosomal replication is complete. To avoid the lethal consequences of such situations, bacteria have evolved replication restart pathways that reload replisomes onto prematurely terminated replication forks. To understand how the primary replication restart pathway in E.