For ectotherms, lifespan is increased at low temperature and decreased at high temperature. A new study in Caenorhabditis elegans shows that thermosensory neurons can counteract the effects of high temperature on lifespan by controlling the activity of a steroid signaling pathway.
In this issue, Xiao et al. challenge the notion that cold temperatures promote longevity solely through thermodynamic effects. They show that low temperatures activate a cold-sensitive cation channel, TRPA-1, which triggers a complex signaling pathway in both neurons and nonneuronal cells to extend the lifespan of Caenorhabditis elegans.
The hypoxic response is a well-studied and highly conserved biological response to low oxygen availability. First described more than 20 y ago, the traditional model for this response is that declining oxygen levels lead to stabilization of hypoxia-inducible transcription factors (HIFs), which then bind to hypoxia responsive elements (HREs) in target genes to mediate the transcriptional changes collectively known as the hypoxic response.(1,2) Recent work in C. elegans has forced a re-evaluation of this model by indicating that the worm HIF (HIF-1) can mediate effects in a cell non-autonomous fashion and, in at least one case, increase expression of an intestinal hypoxic response target gene in cells lacking HIF-1.
The amazing precision with which different cell types find their correct locations in developing tissues has fascinated biologists for decades. Models of cell fate patterning during development emphasize the contrast between spatial gradients of developmental signals that act at long range and cell-to-cell signaling events that act locally. Development of the vulva in the nematode Caenorhabditis elegans provides an elegant model system for examining the patterning of cell fate in an animal. There is strong evidence that two different intercellular signals contribute to the relatively simple induction of cell fate among vulval precursor cells (VPCs): a long-range spatial gradient of epidermal growth factor (EGF) mediated by the EGF receptor (1, 2) and a cell-to-cell lateral signal mediated by the Notch-like receptor LIN-12 (35). It is well established that the combined action of the EGF receptor and LIN-12 receptor signaling pathways generate the pattern of VPCs in the developing vulva (6); however, the molecular details of this cooperative effect have remained elusive. On page 663 of this issue, Yoo et al. (7) provide the missing molecular connection. They report that VPCs activated by a low level of EGF are blocked from adopting a particular cell fate by a LIN-12 lateral signal from a neighboring cell.
The early embryonic development of Nematoda proceeds by three ways, which strictly correspond to three phylogenetic lineages. Under the first way the endodermal precursor is localized in the posterior blastomere at the two-cells stage (such a determination is the peculiarity of all the Chromadoria, including Secernentea and Caenorhabditis elegans). Under the second way the endodermal precursor is localized in the anterior blastomere of the egg. This feature is very unusual for Metazoa, but it is the only way of entoderm determination in all the Dorylaimia orders (Mononchida, Mermithida, Trichinellida, Dioctophymida, Dorylaimida). The third way described for the sea Enoplida is characterized with variable location of blastomers and changeable localization of endodermal precursor before eight-cells stage. It is still unknown of these three variants was typical the most recent common ancestor of present Nematoda. D.A. Voronov (2001) produced argument in favour of variable cleavage as primitive one for Nematoda. This opinion is rejected because of the similarity in development between sea Enoplida and C. elegans. Both of them share such features as low-cell gastrula and neurula, identical phylotypic lima bean stage of embryogenesis, identity of some geometrical figures 4 or 8 blastomers, isolating of the endodermal precursor at the eight-cells stage, the lack in development of any plesiomorphous features, which are widely distributed outside Nematoda (under the variable cleavage of Enoplida there are no such locations of blastomers, which are typical for spiral or radial cleavage, there are no embryonic leaves as well). One can see the homology of separate cells at adult Enoplida and Rhabditia. Cell lineage of Triplonchida as far as it is described at Tobrilus gracilis doesn't exclude the hypothesis on their origin from the cleavage similar to one of present Dorylaimia with localization of the endodermal precursor in the anterior blastomere. In view of all the considerations mentioned above one should interpret variable cleavage of Enoplida as derivation from invariant cleavage