On the cover
Electron micrograph of wild-type Drosophila photoreceptors. Yonamine et al. demonstrate that overexpressing sphingosine kinase 2 causes photoreceptor degeneration and boosts the lysosomal degradation of light-sensing proteins such as Rhodopsin by increasing the levels of dihydrosphingosine 1 phosphate compared to sphingosine 1 phosphate. Image courtesy of Kunio Nagashima, Jairaj Acharya, and Usha Acharya.
See page 557.
- PDF Icon PDF LinkTable of Contents
- PDF Icon PDF LinkEditorial Board
In This Issue
People & Ideas
Alterations in sphingosine kinase activity change the degradation rates of Rhodopsin and the transient receptor potential (TRP) channel by lysosomes and can result in retinal degeneration.
Chromatin structure imposed by condensin II at centromeres enables xHJURP-mediated incorporation of CENP-A.
In the absence of Cbk1 phosphorylation Ssd1-associated mRNAs are redirected from sites of polarized cell growth to stress granules and P-bodies.
Tem1 localization to the spindle pole bodies is essential for mitotic exit and impairs spindle checkpoint function
Alteration of the normal pattern and dynamics of Tem1 localization interferes with spindle checkpoint function and demonstrates that MEN signaling must initiate in the SPBs.
The acetylase inhibitor spermidine and the sirtuin-1 activator resveratrol disrupt the antagonistic network of acetylases and deacetylases that regulate autophagy.
Polycystin-2 goes through the Golgi apparatus when going to the plasma membrane, but bypasses it en route to the ciliary membrane.
The frontotemporal dementia mutation R406W blocks tau’s interaction with the membrane in an annexin A2–dependent manner
The R406W mutation prevents tau from functioning as a linker between the membrane and the microtubule cytoskeleton.
The T cell receptor–activated tyrosine kinase Lck controls docking of the centrosome at the plasma membrane within the immunological synapse but not polarization of the centrosome around the nucleus.
Inhibitory signaling blocks activating receptor clustering and induces cytoskeletal retraction in natural killer cells
Signaling from immunotyrosine-based inhibitory motifs (ITIMs) neutralizes activating signals by inducing a retraction of NK cells from the surface of stimulatory cells.
Binding between the Hedgehog ligand and its receptor Patched 1 is stabilized by Glypican-5.