Time for a quick roundup of today’s new edition of JCB, but, before we get round to the research articles, I’ll point you in the direction of this review on cell polarization in early embryos by Jeremy Nance. It’s the first in a series of “Cell Biology in Development” reviews that we’ll be publishing over the next few weeks and, if you’re attending the upcoming ASCB meeting in Philadelphia, make sure to pick up a copy of our end-of-year special issue, which will contain the entire review series plus a selection of JCB highlights from 2014.
Anyway, on to this week’s highlights: Oas et al. discover a new structure within the nucleus called the B-body, which might serve as a storage depot for proteins that control alternative splicing. As described in this week’s In Focus, the Drosophila RNA-binding protein Arrest accumulates in nuclear B-bodies in flight-muscle founder cells. Following myoblast fusion, Arrest disperses in the nucleus, and directs flight muscle-specific patterns of RNA splicing.
Sainski et al. reveal how an inactive caspase fragment spawned by HIV infection can still kill T cells. The HIV protease cleaves the apoptosis-promoting enzyme caspase 8 to produce an inactive N-terminal fragment. Sainski et al. demonstrate that this fragment can nevertheless bind and activate the pro-apoptotic protein Bak. More here.
Espert et al. identify a phosphatase that helps shut down the spindle assembly checkpoint when chromosomes are correctly attached to the mitotic spindle. As summarized here, the researchers show that the phosphatase PP2A-B56 antagonizes the checkpoint-activating kinase Mps1 by dephosphorylating the kinetochore protein Knl1 in mammalian cells.
Barton et al. identify a last-ditch repair mechanism that enables cells to enter S phase without DNA breaks. The researchers find that DNA damage during G1 spurs the polo-like kinase Plk3 to activate a repair enzyme called CtIP, which initiates a variant version of nonhomologous end joining that repairs complex DNA double-strand breaks in which several DNA injuries are close to one other. As explained here, the study reveals that Plk3 initiates repair of damage caused by certain kinds of radiation, suggesting that inhibiting the kinase might increase the vulnerability of tumors to radiation treatment.
And Vogler et al. describe how the small GTPase Cdc42 and actin-nucleating formin proteins promote lumen formation during Drosophila heart morphogenesis by regulating the dynamics of non-muscle myosin in cardioblasts. You can hear two of the studies authors, Geo Vogler and Rolf Bodmer, describe their findings in this month’s biosights video podcast. Watch below or subscribe in iTunes.
That’s all for today but, as always, you can find all the latest papers by visiting the JCB’s table-of-contents page here.
Cover image showing Arrest (green) in the large nucleus (blue) of a flight muscle founder cell © 2014 Oas et al.