Cellular microbiology

Conversion of PtdIns(4,5)P2 into PtdIns(5)P by the S. flexneri effector IpgD reorganizes host cell morphology.Niebuhr, K. et al. EMBO J. 21, 5069?5078 (2002)

The virulence factor IpgD from Shigella flexneri has been implicated in entry focus formation. Niebuhr et al. now show that IpgD acts as a phosphoinositide phosphatase that dephosphorylates phosphatidylinositol 4,5-bisphosphate. The resulting phosphatidylinositol 5-monophosphate causes a decrease in membrane tether force that eventually promotes membrane ruffling at the entry site ? and thereby increases the pathogen's virulence.

Development

Bicoid associates with the 5′-cap-bound complex of caudal mRNA and represses translation.Niessing, D. et al. Genes & Dev. 16, 2576?2582 (2002) PubMed |

Pattern formation during early Drosophila embryogenesis is initiated by the asymmetric distribution of several transcription factors, including Bicoid (BCD). BCD causes specific translational repression of caudal (cad) mRNA. Translational repression involves not only the binding of BCD to a cis-element in the 3′-untranslated region (UTR) of the mRNA, but also depends ? as Niessing and colleagues now show ? on an eIF4E-binding motif in BCD, which is required for cap-dependent translation initiation. The researchers propose that the 3′-UTR-bound BCD interferes with the assembly of the initiation complex.

Signalling

DAP-kinase induces apoptosis by suppressing integrin activity and disrupting matrix survival signals.Wang, W.-J. et al. J. Cell Biol. 159,169?179 (2002)

Death-associated protein kinase (DAP-kinase), as its name suggests, has a role in apoptosis, which, until now, has remained unclear. This report provides evidence that DAP-kinase exerts an inhibitory effect on integrin function, which negatively regulates integrin-mediated adhesion. Integrin?extracellular-matrix-mediated survival signals are consequently suppressed, which, through the activation of p53-dependent pathway, induces anoikis-like apoptosis.

Replication

De novo formation of centrosomes in vertebrate cells arrested during S phase.Khodjakov, A. et al. J. Cell Biol. 158, 1171?1181 (2002)

Centrosomes replicate through a semiconservative mechanism, and their number is controlled by the cell's ploidy. Earlier studies had suggested that centrosomes do not regenerate, and that centrosome assembly requires a specific 'template'. However, Khodjakov and colleagues now show that when centrosomes are destroyed by laser surgery in CHO cells arrested in S phase, new centrosomes form de novo. Pericentriolar material appears after 5?8 hours, and centrioles by 24 hours.