Volume 11 Issue 1, January 2009

Most cells can rapidly repair extensive tears in their plasma membrane, a response dependent on extracellular calcium. Entry of extracellular oxidants through a membrane disruption oxidizes and thus activates a newly discovered membrane repair protein, MG53, in skeletal muscle cells.

Septins comprise a conserved family of cytoskeletal proteins distinct from the microfilament, microtubule and intermediate filament systems. They are GTPases that have been implicated in a number of cellular processes ranging from mitosis to vesicular trafficking. A new study identifies a previously undefined role for septins as cellular 'corsets', modulating cell shape and providing cortical rigidity in T cells that allows for their controlled migration.

Induction of apoptosis causes active dissipation of the RanGTP gradient across an intact nuclear envelope by immobilizing RCC1, the guanine nucleotide exchange factor for RanGTPase, on chromatin. The subsequent reduction in nuclear trafficking prevents the movement of NF-κB into the nucleus, thereby allowing apoptosis to proceed.

Secreted Frizzled-related proteins (sFRPs) are signalling molecules well-known as antagonists of the Wnt pathway, but recent studies indicate that they may have additional functions unrelated to Wnt. A new study demonstrates that mammalian sFRP2 can act as an enhancer of collagen processing in vitro and in vivo, augmenting myocardial injury-driven fibrosis. These findings underscore the biological versatility of sFRP family members.

Septins are cytoskeletal proteins that form a ring at the cytokinetic furrow. Now an analogous 'molecular corset' of septins is found to be required for T lymphocyte migration.

Incorrectly oriented chromosomes in mitosis can lead to chromosome instability and aneuploidy. The kinesins Kif2b and MCAK stimulate kinetochore-microtubule dynamics to correct mis-orientations.

The guanine nucleotide exchange factor for Ran, RCC1, dynamically binds chromatin. During apoptosis, caspase-mediated activation of Mst1 induces histone H2B phosphorylation, which immobilizes RCC1 on the chromatin, leading to a reduction in nuclear RanGTP.

Secreted frizzled-related proteins (sFRPs) were reported to antagonise Chordin processing by Sizzled, a tolloid-like metalloproteinase in Xenopus and zebrafish. Surprisingly, mammalian sFRP2 enhances the activity of tolloid-like metalloproteinases on procollagen C to modulate fibrosis associated with cardiac injury.

A phosphatidylserine-binding protein, MG53, is shown to participate in membrane repair. MG53 recruits vesicles to the repair site in an oxidation dependent manner and MG53-null mice develop progressive myopathy associated with defective membrane repair.

The midbody ring connects two dividing cells at the end of cytokinesis. Depletion of autophagy components or inhibition of lysosomal function result in accumulation of midbody rings.

In cytokinesis, formation of the contractile ring depends on localized activation of RhoA at the cell equator. This study demonstrates that GAP activity of MgcRacGAP is necessary throughout cytokinesis to maintain a focused zone of Rho activity.

As the root develops, auxin transport through non-hair cells sustains root-hair outgrowth. Mathematical modelling and experimental data reveal that auxin is transported through canals across the non-hair cells.

The ubiquitin ligase Siah2 targets HIPK2 kinase for degradation during hypoxia. During normoxia, however, the kinase is stable, as phosphorylation of Siah2 by HIPK2 weakens the interaction.

Doubled-stranded DNA breaks activate ATM kinase, precipitating a DNA damage response. The nucleosome-binding protein HMGN1 governs ATM activation by inducing H3K14 acetylation, which regulates chromatin binding of ATM both before and after DSB formation.

The prolyl isomerase Pin1 acts in various cellular processes. It has now been implicated in telomere maintenance by regulating the stability of the telomere binding protein TRF1.