New issue: October 5th 2009

Time for a quick rundown of highlights from the latest issue of the JCB...

Our cover image this week is a section through a mouse whisker, stained in red for Merkel cells, which transmit mechanical stimuli to sensory neurons (stained in green). In other words, Merkel cells are involved in touch sensation, but the embryonic origin of these cells was unclear, since they have characteristics of both epidermal and neuronal cell types. In this issue, Van Keymeulen et al. demonstrate that they arise from epidermal progenitors during both embryogenesis and adult homeostasis. Moreover, deletion of a transcription factor called Atoh1 in these cells completely prevents Merkel cell development. You can read more in this summary, including why these findings may shed light on a particularly aggressive cancer that arises from Merkel cells.

Meanwhile, our In Focus for this issue centers on a study from Sivaramakrishnan and Spudich that reveals how multiple myosin motors coordinate their activities to transport vesicles along the actin cytoskeleton. The researchers use a combination of experimentation and computer modeling to show that even monomeric myosins (which would be completely unable to move cargo on their own) can join forces to carry the load.

Switching to mitosis, O'Connell et al. use a fascinating cell biological phenomenon called MUG to unpick the contributions that kinetochores and chromatin make to the assembly of the mitotic spindle. MUG stands for Mitosis with Unreplicated Genomes, and is induced by the prolonged treatment of cells with hydroxyurea. The fascinating thing is that these cells form a normal mitotic spindle attached to kinetochores and centromeric DNA aligned at the metaphase plate. Yet the rest of the cell's (unreplicated) chromatin is pushed out to the cell periphery. As you can read in this summary, O'Connell et al. use these cells to show that kinetochores alone can direct spindle assembly without the help of a Ran-GTP gradient generated from the bulk chromatin.

Meanwhile, McCleland et al. block DNA replication in early stage Drosophila embryos to demonstrate that S phase controls the speed at which the embryonic nuclei enter mitosis. Earlier this year, the researchers used the same experimental system to observe the contributions of cyclins to mitotic progression. I won't go into any more detail here, as Eun Choi has produced an extra special edition of biosights that covers both papers and features interviews with both Mark McCleland and Pat O'Farrell. Eun even made a trip to UCSF to film the researchers at work - you can see the video by clicking here, or by watching below:

Staying with flies, Shen and Ganetzky show how autophagy promotes Drosophila synapse development. You might think of autophagy as being a destructive pathway, but it actually plays a constructive role at neuromuscular junctions by counteracting proteosome-mediated degradation. Flies overexpressing the autophagy protein Atg1 have larger NMJs because they destroy an E3 ubiquitin ligase that would otherwise limit synaptic size. As I explain in this summary, the authors believe autophagy is a great way for neurons to regulate synaptic plasticity in response to many different environmental stimuli.

Meanwhile, Massaro et al. reveal a signaling pathway that helps neurons maintain synaptic structure despite environmental stress. MAPK-JNK-Fos signaling rescues NMJ stability to prevent disruption of the neuronal cytoskeleton from causing synapse disassembly.

Finally for today, we have two papers that investigate the structures of protein particles transported back and forth along the length of cilia and flagella. Bidirectional transport of these particle trains is essential for assembling and maintaining flagella. Pigino et al. provide a beautiful electron-tomographic analysis of the "trains" of particles heading in both the anterograde and retrograde directions. Particle trains heading to the tip of the flagellum (indicated with a black arrowheads in the image to the right) are longer and narrower than trains returning to the organelle's base (white arrowhead).

How do cells control the size of cilia and flagella? Engel et al. demonstrate that trains traveling to the flagella tip are smaller in longer cilia. As the group's modeling shows, this may help the organelle to keep a consistent length, as the assembly rate will decrease as the cilia/flagella grows larger.

Plenty more in elsewhere in this issue. As always, you can find the full table of contents by clicking here.