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[Figure][1] EGF spurs control cells (top) to extend protrusions but not cells that carry an unphosphorylatable form of Arp2/3 (bottom). [LeClaire et al.][2] identify a kinase that helps activate the actin-nucleating Arp2/3 complex. The Arp2/3 complex spurs membrane protrusion and cell

Cdk5 is a kinase expressed mainly in neurons, where it helps regulate the activity of a whole host of downstream targets, including ion channels and synaptic scaffold proteins. Thus, it’s perhaps to be expected that Cdk5 dysregulation is associated with many neuropathologies (1). Li-Huei Tsai PHOTO COURTESY OF LEN RUBENSTEIN Li-Huei Tsai cloned Cdk5 as a postdoc (2) and decided she wanted to study it further in her own lab. When asked during job interviews what she would do if Cdk5 wasn’t involved in any interesting phenotypes, she replied that she would no doubt find something else interesting to study. She was soon hired on at Harvard. As it turns out, though, Cdk5 (and its regulation) is plenty interesting (3–5), as we learned when we called her at her current lab at the Massachusetts Institute of Technology.

[Figure][1] Larval fat bodies expressing cleavage-resistant Acinus (right) contain more autophagosomes (green) than control fat bodies (left). Nandi et al. describe how a caspase and a kinase combine to regulate the levels of a protein that stimulates autophagy. During autophagy, double

[][1] A kinase-dead Ire1 (right) is resuscitated by 1NM-PP1. Papa/AAAS A new output mode for a kinase is reported by Feroz Papa, Peter Walter, and colleagues (HHMI and University of California, San Francisco [UCSF], CA). They find that, for Ire1 kinase, the key to activation is not

A kinase that arrests cells in response to nuclear DNA damage also safeguards the inheritance of mitochondrial DNA (mtDNA), [Crider et al.][1] report. mtDNA encodes many of the proteins required for mitochondrial respiration. Budding yeast lacking mtDNA can still survive, but Crider et al. found

A lone amino acid change determines success or failure for strains of Toxoplasma gondii , say [Yamamoto et al.][1] The group identifies a kinase mutation that thwarts one strain's ability to activate Stat3 and halt the host immune response. ![Figure][2] A polymorphism in the Toxoplasma

[Graphic][1] Salt stress fragments wt (top) and yck3 Δ (bottom) vacuoles (middle panels), but yck3 Δ vacuoles then prematurely reassemble (right panels).On [page 401][2], LaGrassa and Ungermann show that divided vacuolar membranes are kept apart by a kinase that disables their

[Graphic][1] AKAP79 (blue) brings SAP97 (green) to the plasma membrane (bottom), where they also associate with CaN and PKA.Opposites really do attract. Results on [page 101][2] by Oliveria et al. show that, although they perform opposing functions, a kinase and a phosphatase