Reviews & Analysis

Cytoplasmic processing bodies, also known as P-bodies, concentrate enzymes that are involved in mRNA turnover and sequester mRNAs away from the translational machinery. Strong evidence now connects the RNA interference machinery with P-body formation.

New work reveals a key signal transduction pathway through which nitric oxide (NO) regulates apoptosis induced by disparate cellular stresses. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is S-nitrosylated by NO, which initiates an interaction with the E3 ligase Siah1, leading to nuclear translocation and ubiquitin-mediated degradation of nuclear target proteins.

The small GTPase Ran controls nucleocytoplasmic transport and has multiple roles during cell division. A new study has identified the nuclear export factor Crm1 as a mitotic effector of Ran-GTP at kinetochores, where it has a role in microtubule attachment.

A recent study has shown that the Ssl1 subunit of the general transcription/DNA repair factor TFIIH contains ubiquitin ligase activity that is dependent on a RING domain. The RING domain is required for transcription of a subset of yeast genes that are involved in DNA damage repair, thus uncovering a novel ubiquitination-associated function for TFIIH in the repair process.

How cells disassemble their focal adhesions is not well understood. Now, Ezratty et al. have shown that the GTPase dynamin acts after microtubule targeting of focal adhesions to trigger their disassembly. One intriguing possibility is that dynamin might drive disassembly through endocytosis.

It has long been known that the mammalian small GTPase Rab5 is involved in clathrin-mediated endocytosis. However, most Rab5-interacting proteins are localized to endosomes rather than to the plasma membrane. A newly discovered nucleotide-exchange factor for Rab5 in Caenorhabditis elegans now provides the missing link for activating Rab5 at the plasma membrane.

Factors that determine whether precursor cells will differentiate into adipocytes remain poorly understood. A systematic evaluation of gene expression in cells with a continuum of differentiation potentials has confirmed the importance of certain pathways and has identified a novel regulator of brown adipogenesis.

Talin is a core component of the integrin adhesion complex. It is now shown that talin also regulates transcription, an activity that is apparently independent of its interaction with integrins. Talin represses the expression of Drosophila melanogaster DE-cadherin through an unknown molecular mechanism.

Conditional knockout of the KAP3 subunit from the kinesin motor KIF3 alters tissue patterning and causes abnormal proliferation of neural progenitor cells in the mouse brain. Impaired transport of N-cadherin to the surface of these cells may be one explanation for how such defects arise.

Highly localized Ca²⁺ signals called Ca²⁺ sparks have been widely reported in all mammalian muscle types except adult skeletal muscle. We now learn that these mysteriously absent sparks can be seen during stress or disease, raising the question of how these signals become unmasked in these conditions.

By what molecular mechanisms do microtubules regulate the spatial distribution of actin assembly in cells? In fission yeast, a novel SH3-domain-containing protein, Tea4p, acts to bridge the microtubule plus-end-binding protein Tea1p with the actin-nucleating formin protein For3p.

Vesicle formation at the trans-Golgi network may be mechanistically more similar to endocytic vesicle formation at the plasma membrane than previously thought. Both processes share common components including the dynamin-binding protein cortactin.

The HIV type 1 (HIV-1) life-cycle involves a number of cellular cofactors. Some are essential for HIV-1 replication and thus may serve as targets for therapeutic intervention. An emerging role for cellular DNA repair in HIV-1 infection suggests that inhibition of these repair functions may lead to suppression of viral replication.

Phosphorylation of synaptojanin 1 by the EphB2 receptor tyrosine kinase is a molecular switch. This phosphorylation prevents the interaction of synaptojanin 1 with endophilin and promotes endocytosis. Subsequent dephosphorylation initiates an interaction with endophilin, leading to clathrin uncoating and fusion with endosomes.

All members of the conserved family of structural maintenance of chromosomes (SMC) proteins are essential for cellular viability. The Smc1–Smc3 heterodimer is a constituent of cohesin and Smc2–Smc4 of condensin, which are both required for proper chromosome distribution at mitosis. Now, the third SMC heterodimer, Smc5–Smc6, which had previously been implicated only in DNA repair, also turns out to be crucial for chromosome segregation.