In today’s new issue of JCB, Hégarat et al. describe how the Aurora family of protein kinases regulates chromosome and microtubule dynamics in mitosis. Cells lacking either Aurora A or Aurora B fail to properly align their chromosomes on the mitotic spindle, resulting in chromosome mis-segregations. As described in this summary, cells lacking Aurora A AND Aurora B, on the other hand, fail to depolymerize spindle microtubules in anaphase, preventing sister chromatid separation.
Schmidt et al. describe a signaling pathway that helps embed acetylcholine receptors in the post-synaptic membrane of neuromuscular junctions. Neuregulin signaling molecules bind to their ErbB receptors and induce the phosphorylation of a post-synaptic scaffold protein called alpha-dystrobrevin1, which stabilizes acetylcholine receptors at the post-synapse to maintain proper synaptic neurotranmission. As explained in this week’s In Focus, the signaling pathway seems to particularly affect acetylcholine receptors that have undergone a round of endocytic recycling, though why this population of receptors behaves differently isn’t clear. Meanwhile, Baez et al. describe how cytoplasmic RNA granules regulate post-synaptic remodeling. The researchers identify S-foci, which contain the translational repressor Smaug1 and which regulate the local translation of mRNAs encoding proteins (e.g. CaMKinaseII) in response to NMDA receptor stimulation.
Emond et al. reveal a new way for cells to adhere to each other. Though classical cadherins like E- and N-cadherin are known to mediate intercellular adhesion, the role of the related protocadherin proteins in holding cells together is much less clear. Emond et al. find that Protocadherin-19 becomes adhesive when it forms a complex with N-cadherin, so that it forms homophilic adhesions between neighboring cells. N-cadherin switches on Protocadherin-19’s adhesive properties, but it doesn’t mediate the intercellular adhesion itself. More here.
Sideridou et al. report that Cdc6, a protein that permits cells to replicate their DNA, also induces epithelial to mesenchymal transitions by shutting down the expression of E-cadherin. Cdc6 overexpression may therefore aid the progression of cancer by stimulating both DNA synthesis and metastasis. You can find a longer summary here.
And Nekrasova et al. reveal that the two types of cadherin molecules that assemble into desmosomal adhesions are transported to the plasma membrane by two distinct kinesin motors. You can learn more in this month’s biosights, in which senior author Kathleen Green explains why using two independent transport mechanisms to build desmosomes might allow cells to tailor the strength of their adhesions during development and disease.
That’s all we have time for today, but you can find lots of other interesting papers in today’s new issue by visiting the table of contents here.
Cover image courtesy of Nadia Hégarat and Helfrid Hochegger.