New issue: May 14th

In today’s new issue of JCB, Mitra et al. reveal how mitochondrial morphology regulates the development of Drosophila egg chambers. Egg chamber follicle cells lacking the mitochondrial fission protein Drp1 maintain a highly-fused mitochondrial network and hyperproliferate instead of exiting the cell cycle and terminally differentiating. Depleting the mitochondrial fusion protein Marf-1, on the other hand, causes follicle cells to differentiate prematurely. Senior author Jennifer Lippincott-Schwartz explains in this summary that mitochondrial morphology might be linked to differentiation because cells’ energetic requirements change when they exit the cell cycle. Meanwhile, Kageyama et al. demonstrate that mouse neurons lacking Drp1 die because their mitochondria fuse and accumulate oxidative damage.

Shevchuk et al. use ion conductance microscopy – a technique that rapidly scans the topography of the plasma membrane – to examine how clathrin-coated pits close as they internalize from the cell surface. (If you haven’t heard of ion conductance microscopy before, the authors provide a nice explanation at the start of their Materials and Methods section). Clathrin-coated pits are generally thought to seal off from a flat region of the plasma membrane, but Shevchuk et al. find that 70% of them are capped by a membrane protrusion that grows from one side of the pit. You can read about the differences between these two mechanisms of pit closure in this summary.

Wei et al. identify an miRNA family that inhibits the differentiation and proliferation of bone-forming osteoblasts. miR-34b and miR-34c decrease bone formation in mice by reducing levels of the osteoblast differentiation factor Satb2 and the cell cycle proteins Cyclin D1, CDK4, and CDK6. As explained in this week’s In Focus, though miRNAs have been implicated in bone formation before, this is the first in vivo study of how individual miRNAs regulate osteoblast differentiation.

Oikawa et al., on the other hand, study the differentiation of bone-resorbing osteoclasts. This process involves the fusion of precursor cells to form mature, multi-nucleate osteoclasts (such as the one pictured on this week’s cover, for example). Oikawa et al. reveal that osteoclast cell fusion is mediated by invasive, podosome-like protrusions that are formed by the phospholipid-binding adaptor protein Tks5. More here. 

There’s lot’s of other great papers that you can find on our table of contents, but I’ll leave you today with a link to this month’s biosights video podcast, in which Ryan Petrie describes a new way that fibroblasts migrate through three-dimensional environments.  As revealed in this paper, depending on the strength of intracellular RhoA signaling and on the elastic behavior of the extracellular matrix, fibroblasts can form blunt, cylindrical protrusions called lobopodia instead of thin, wide lamellipodia-like extensions.

If you work in a cell migration lab and would like to discuss Petrie et al.’s study with your colleagues, you can download a “Journal Club Pack” for the paper by clicking here.

Cover image courtesy of Tsukasa Oikawa.