Volume 11 Issue 7, July 2009

Errors in chromosome–spindle attachments during cell division can lead to an irreversible change in chromosome number. Proper connections between chromosomes and spindle microtubules can be promoted by both chromosome-intrinsic and extrinsic mechanisms during mitosis and meiosis.

SDPR is a new regulator of caveolae biogenesis. SDPR overexpression results in increased caveolae size and leads to the formation of caveolae-derived tubules containing Shiga toxin. SDPR may therefore be a membrane curvature-inducing component of caveolae.

In the Notch pathway, the transmembrane ligand Delta is internalized and then re-established on the surface of signal-sending cells to allow the productive binding and activation of the Notch receptor on neighbouring cells. Arp2/3-dependent actin polymerization directs Delta trafficking through this circuit.

For nucleosome-encoded epigenetic information to be transmitted, an epigenetic mark requires a 'reader' for its physical recognition. CENP-N has now been identified as a reader of the centromere-specifying epigenetic mark that is generated by incorporation of the histone H3 variant CENP-A into centromeric nucleosomes.

The cortical microtubule array in plants orients nascent cellulose fibrils by organizing cellulose synthase complexes in the plasma membrane. Microtubules are now shown to facilitate the delivery of these complexes to the plasma membrane through their depolymerizing ends.

Caveolae are plasma membrane invaginations implicated in endocytosis. SDPR is a new component of caveolae that facilitates membrane curvature, caveolae formation and tubulation induced by extracellular ligands such as Shiga toxin B.

Cell fate decisions mediated by Notch signalling generally involve direct cell–cell contact between adjacent cells. A new Arp2/3-dependent actin structure directs the Notch ligand Delta to microvilli in signal-sending cells during sensory organ development in fly.

During centriole duplication, a new centriole of defined length forms adjacent to the pre-existing centriole. The centriolar protein CPAP is under tight cell-cycle control and controls centriole length through its intrinsic tubulin-dimer binding activity.

Mitotic chromosome congression is thought to require microtubules attached end-on to kinetochores (K-fibres). In human cells lacking K-fibres, chromosomes congress by the gliding of unattached kinetochores along microtubule bundles, driven by the plus-end kinesin motor CENP-E.

Female meiosis occurs without centrosomal microtubule organization. In C. elegans oocytes, microtubule bundles surround homologous bivalent chromosomes. The chromokinesin KPL19 is concentrated in a ring around each bivalent and drives metaphase alignment through a polar ejection force.

Plants show distinct morphologies in different light conditions through a process called photomorphogenesis. A predominant feature of photomorphogenesis is the reduced growth of seedlings under light conditions compared with darkness. For this adaptive event, the most well-known molecular mechanism involves photoreceptor-mediated inhibition of cell elongation^1,2,3,4. However, it is not known whether additional pathways exist. Here, we describe a newly discovered pathway of light-modulated plant growth mediated by the halotolerance protein HAL3, a flavin mononucleotide (FMN)-binding protein involved in cell division^5,6,7,8. We found that light, especially blue light, suppresses growth of rice seedlings by reducing the activity of Oryza sativa (Os) HAL3. Both in vitro and in vivo studies showed that OsHAL3 is structurally inactivated by light through photo-oxidation and by direct interaction with photons. In addition, the transcriptional expression of OsHAL3 is synergistically regulated by different light conditions. Further investigation suggested that OsHAL3 promotes cell division by recruiting a ubiquitin system, rather than by its 4′-phosphopantothenoylcysteine (PPC) decarboxylase activity. Our results uncover a new mechanism for light-regulated plant growth, namely, light not only inhibits cell elongation but also suppresses cell division through HAL3 and E3 ubiquitin ligase. This study thus brings new insights into our understanding of plant photomorphogenesis.

Overexpression of the mitochondrial matrix-localized protease PaLON in Podospora anserina reduces levels of carbonylated and carboxymethylated proteins, resulting in a higher resistance to oxidative stress and an extended life span.

Drosophila germ-band extension is thought to rely mainly on cell intercalation events. Quantitative analysis of cell shape changes and movements show that extrinsic tensile forces generated by the invaginating mesoderm drive cell shape changes to participate in this elongation.

Chromatin decondensation is required for repair factors to access damaged DNA. BRIT1/MCPH1, a damage response protein mutated in microcephaly, recruits the chromatin remodelling complex SWI/SNF to sites of DNA damage after phosphorylation by ATM/ATR. This mechanism is critical for efficient DNA repair and survival.

The secreted factor EGFL7, which is known to regulate cell migration and angiogenesis, is expressed in the brain where it binds receptors of the Notch family. Binding decreases Notch signalling, inhibits self-renewal of neural stem cells in culture and affects proliferation and differentiation of adult neural stem cells.

How TGF-β activates Akt in disease situations is unclear. By acting on the promotor of RP23, a non-coding RNA which encodes two microRNAs, TGF-β signalling downregulates the phospatase PTEN, a target of these microRNAs and an inhibitor of Akt signalling.

The wound-healing transcription factor Grainy head upregulates a receptor tyrosine kinase of the Ret-family, Stitcher. Stitcher orchestrates re-epithelialization by triggering rearrangements of the actin cytoskeleton and changes in gene expression through Erk phosphorylation and regulation of Grainy head activity.

The histone H3 variant CENP-A specifies centromere identity. CENP-N is the first selective binding partner of CENP-A. Inhibition of CENP-N binding to CENP-A or CENP-N depletion prevents the recruitment of the other CENP proteins involved in centromere assembly.

Inflammatory breast cancer rapidly metastasizes. Overexpression of the translation factor eIF4GI increases translation through the activation of internal ribosome entry sites. Members of the p120 family of catenins are key targets involved in metastasis deregulated in this way.

Intracellular tau inclusions, a hallmark of several neurodegenerative diseases, propagate in the brain in an unknown fashion. Brain extracts prepared from mice expressing mutated human tau injected into mice expressing wild-type human tau induce the formation and spread of wild-type human tau inclusions.