In today’s new edition of JCB, Schouteden et al. reveal that the ciliary transition zone promotes cell adhesion. The transition zone lies between the cilium’s basal body and its microtubule-based axoneme. As explained in this week’s In Focus, Schouteden et al. disrupt this structure in C. elegans, and find that worm neurons are still able to assemble ciliary axonemes, but are unable to extend dendrites, due to a defect in cell-matrix adhesion.
Marshall et al. show that recycling endosomes help cytotoxic T cells kill pathogens and tumor cells by delivering the SNARE protein syntaxin-11 to the immunological synapse where the T cell contacts its target. As summarized here, cytotoxic granules can then fuse and release their contents at this site in order to kill the target cell.
Lim et al. show that hydrogen peroxide at the centrosome spurs cells to advance through mitosis. As described here, hydrogen peroxide levels rise as cells enter mitosis, deactivating the centrosome-localized phosphatase Cdc14B that would otherwise drive immediate mitotic exit. Later in mitosis, cells activate the enzyme peroxiredoxin I at centrosomes in order to lower hydrogen peroxide levels and allow Cdc14B to do its work.
Meanwhile, Lambrus et al. demonstrate that p53 guards the genome by preventing cells with abnormal numbers of centrosomes from dividing. In the absence of p53, cells can continue dividing without centrosomes, resulting in chromosome mis-segregation. More here.
And Lerit et al. describe how a scaffold formed by the proteins centrosomin and PLP maintains the activity of interphase centrosomes in early Drosophila embryos, which is essential for both nuclear spacing and proper chromosome segregation. The authors discuss their work in this month’s biosights podcast, which you can watch below or subscribe to in iTunes.
That’s all for today but, as always, you can discover plenty of other interesting papers by visiting our table of contents page here.
Cover image showing the structure of the ciliary transition zone © 2015 Schouteden et al.