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Architecture of gap-junction net-works in the cochlea of a guinea-pig organ of Corti. Connexin 26 expression is shown superimposed onto the staircase designed by architect and designer Antoni Gaudi Cornet (www.sagradafamilia.org/eng/index.htm ). The coiled shape of the staircase recalls that of the mammalian auditory organ (www.vimm.it/cochlea). cover design: Lawrence Keogh
Some Drosophila neural progenitor cells generate segment-specific lineages in the thorax versus the abdomen. The basis for these differences is the differential expression of Cyclin E. Cyclin E functions downstream of the homeotic genes and largely independently of its role in proliferation to autonomously specify thoracic identity.
Accurate chromosome segregation occurs during each cell division and is orchestrated by the dynamic microtubules of the mitotic spindle. Our understanding of this process has increased severalfold with the elucidation of the molecular components that coordinate microtubule flux.
Regulating actin dynamics through cofilin dephosphorylation is the role of a newly identified phosphatase, chronophin, a member of the haloacid dehalogenase (HAD) superfamily. Chronophin, the second cofilin phosphatase to be identified, has high phosphoprotein specificity towards cofilin, but curiously it was also discovered independently as a pyridoxal phosphate (vitamin B6) phosphatase.
Nuclear pore complexes intuitively seem functionally analogous to transmembrane channels. Recent bioinformatic analysis, however, suggests a quite different evolutionary relationship: one between nuclear pore complexes and vesicle coat components. This has led to the provocative hypothesis that these distinct structures share a common role in bending membranes.
The activation and targeted localization of ubiquitin E2 conjugating enzymes could provide a point for regulating ubiquitin-dependent cell functions. Supporting this view, the ubiquitin charging and activation of a class of E2 enzymes has been directly linked to their nuclear import.
Genetic studies have conclusively linked connexin channels to human diseases, but the nature of the signals that are disrupted by channel mutations has remained elusive. A recent study has taken advantage of a deafness-causing mutation to suggest that permeability to inositol trisphosphate, the Ca2+-mobilizing messenger, is crucial for normal hearing.