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In the second Review in our Genomic Instability series, Rudolph and colleagues discuss how the genomic damage that accumulates during ageing affects stem cell function through both cell-intrinsic and cell-extrinsic mechanisms.
Collective cell migration depends on multicellular mechanocoupling between leader and follower cells to coordinate traction force and position change. Co-registration of Rho GTPase activity and forces in migrating epithelial cell sheets now shows how RhoA controls leader–follower cell hierarchy, multicellular cytoskeletal contractility and mechanocoupling, to prevent ectopic leading edges and to move the cell sheet forward.
Correct regulation of insulin secretion by the pancreas is crucial for organismal function and survival. The AMPK-related kinase SIK2 (salt-inducible kinase 2) is now shown to be stabilized in pancreatic β-cells following glucose stimulation, leading to improved systemic glucose homeostasis by regulating cellular calcium flux and insulin secretion.
Defective asymmetric cell divisions of stem and progenitor cells are associated with tumorigenesis by a largely unknown mechanism. A signalling axis involving Snail, microRNA-146a and Numb is now shown to regulate the switch between symmetric and asymmetric cell division in colorectal cancer stem cells.
Silberzan and colleagues demonstrate that local RhoA activity and mechanical forces control the formation of 'migration fingers', cell protrusions involved in the leader-cell-driven collective migration of epithelial cell monolayers.
How sensory neurons integrate mechanical signals during touch sensation has remained unclear. Using a combination of laser axotomy and FRET imaging to measure force across single cells and molecules, Goodman and colleagues show that the neuronal spectrin cytoskeleton transduces touch sensation in C. elegans.
Screaton and colleagues delineate a pathway involving the AMPK-related Sik2 kinase using mouse models. They show that Sik2-mediated phosphorylation and subsequent degradation of CDK5R1 (p35) by PJA2 is needed for glucose-induced insulin secretion and β-cell functional compensation in models of hyperglycemia and obesity.
Ma and colleagues report that in E-cadherin-deficient basal-like breast cancer cells, α-catenin acts as a tumour suppressor by interacting with and stabilizing IκBα, leading to inhibition of NF-κB signalling.
Hebrok and colleagues use mouse models to demonstrate that loss of the chromatin modifier Brg1 cooperates with oncogenic KRas to form lesions resembling intraductal papillary mucinous neoplasia that progress to pancreatic adenocarcinoma.
Wang, Yang and colleagues delineate a Snail-β-catenin-miR-146a signalling axis that directs a switch from asymmetric to symmetric cell division, resulting in colorectal cancer stem cell expansion.
Groth and colleagues identify proteins associated with newly synthesized DNA — isolated by nascent chromatin capture — as well as proteins associated with mature DNA, and find factors not previously linked to replication or nascent chromatin.
