[
Nat Genet,
1992]
Predicting coding regions from genomic sequence is not entirely accurate, and predicting expression patterns of candidate genes is still a fantasy. Both of these concerns can be addressed by analysing expressed sequences (cDNA) in addition to genomic sequences. The genomic sequencing of the nematode Caenorhabditis elegans has begun; in parallel, several groups (including the genomic sequencing participants) are isolating, sequencing and mapping C. elegans cDNA clones. The first results of this endeavor, including the analysis of about 1,600 independent cDNA sequences, appear in this issue.
[
Nature,
1999]
Advances in human genetics have meant that the genes mutated in human diseases can be identified exclusively by their location in the genome. But how do we work out the cellular functions of the associated protein products? Reports on pages 383 and 386 of this issue begin to address this problem for two proteins - polycystin-1 (PKD1) and polycystin-2 (PKD2) - that are defective in human kidney disease. From their studies of the nematode worm Caenorhabditis elegans, Barr and Sternberg present evidence that homologues of the polycystins act together in a signal-transduction pathway in sensory neurons. Chen et al., by contrast, have used an oocyte-expression system in the from Xenopus laevis to show that a homologue of PKD2 is associated with the activity of a cation channel. These results support the hypothesis that polycystin-related proteins belong to a hitherto unknown class of signal-transduction molecules.
[
Nature,
1993]
Twenty years ago Sydney Brenner described an electrode-less plan for attacking the problems of neural development and physiology in the small nematode Caenorhabditis elegans. He proposed to set the groundwork by reconstructing the entire nervous system of the worm by serial section electron microscopy. Given the resulting wiring diagram, he thought it might be possible to make guesses as to how the nervous system worked. A second aspect of his plan was genetics: single-gene mutants exhibiting aberrant behaviour, such as uncoordinated movement, were to be analysed to address the question of how genes specify development and function of the nervous system. In two papers beginning on page 334 of this issue, McIntire et al. demonstrate that work on Brenner's plan, with a few tricks added over the years, is progressing very nicely.