CZ4734

Caenorhabditis elegans

CZ4733

Caenorhabditis elegans

Olson EN et al. (1992) Curr Biol "MyoD and the paradoxes of myogenesis."

Olson EN, Perry WM

[Curr Biol, 1992]

When the mammalian skeletal-muscle-specific transcription factors MyoD, myogenin, myf5 and MRF4, were first identified and shown to have the potential to activate myogenesis in nonmyogenic cell types, the molecular basis for establishment of the muscle phenotype seemed satisfyingly simple. These proteins share a 70-amino-acid region of homology that encompass a basic-helix-loop-helix (BHLH) motif that mediates oligomerization and binding to a conserved DNA sequence. That this conserved sequence is associated with most muscle-specific genes, seemed sufficient to explain the mechanism for activation of the set of genetically unlinked genes that is induced during myogenesis...

CZ5847

Caenorhabditis elegans

CZ9236

Caenorhabditis elegans

Boris Shtonda et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "Blue light avoidance and sensitivity in C.elegans."

Boris Shtonda, Leon Avery

[Neuronal Development, Synaptic Function, and Behavior Meeting, 2006]

It is generally believed that C.elegans is not sensitive to the human-visible light. We have found two novel light responses in worms: light avoidance and light sensitivity. For light avoidance, we developed two assays: an acute avoidance assay and a dispersal assay. In the former, the latency of the backing response upon light stimulation is scored; in the latter, worms" dispersal from the central illuminated area of the plate to the shadowed periphery is quantified. In both assays, responses to the blue part of the human-visible spectrum (400-500 nm) were far more pronounced than to the green (500-550 nm); responses to red light (above 600 nm) were undetectable. This wavelength specificity strongly suggests that this response is not heat avoidance. If it were heat avoidance, a much stronger correlation with the light intensity, rather than wavelength, would be expected. In addition, we used a small temperature probe to confirm that heating of the plate did not occur at light intensities used. To elicit acute avoidance, a blue light intensity of 2000 Wm-2 was needed (about twice that of sunlight), while dispersal was observed starting at 200 Wm-2. The light sensitivity phenotype was studied by continuously illuminating animals at different stages of development. Blue light (450-490 nm) of 100 Wm-2 arrested egg development and caused a growth delay in larval development. Higher intensities caused other distinct phenotypes: arrest of pharyngeal pumping, developmental arrest, and, finally, death. In attempt to identify neurons involved in light avoidance, we laser ablated dye-filling neurons: ASH, ADL, ASI, ASK and ASJ; all together or in subsets, and in all cases, performance in the acute avoidance assay was normal. This was consistent with a normal performance of amphid-defective mutants, osm-6, osm-2 and che-2, in the light dispersal assay. (Amphid-defective mutants were previously found to be defective in temperature avoidance). We found, however, that worms lacking TAX-2, a worm ortholog of the vertebrate rod photoreceptor cyclic nucleotide gated channel, were defective in light dispersal. In addition to amphid neurons, tax-2 is also expressed in the neurons exposed to the body cavity, where it is involved in social and oxygen avoidance behaviors and is activated by soluble guanylyl cyclases (sGCs). We are currently testing whether tax-2 also functions in these neurons to mediate light avoidance. sGCs are hemoproteins, and therefore may be direct light targets.

Hubbard EJA et al. (1998) East Coast Worm Meeting "Genetic Analysis of Gonadogenesis in C. elegans"

Greenwald IS, Temkin I, Hubbard EJA

[East Coast Worm Meeting, 1998]

Gonadogenesis, the formation of the somatic gonad and the germ line, is an excellent model for the study of diverse biological phenomena such as cell-cell interactions, cell fate specification, stem cell maintenance, differentiation, morphogenesis, and cell migration. Based on previous observations on existing collections of temperature sensitive lethal mutants with defects in gonadogenesis (see 1995 WM abstract), we tailored our genetic strategy to allow for the isolation of mutations in genes required at embryonic and early larval stages as well as during gonadogenesis. We have isolated alleles representing a variety of classes of mutant phenotypes, including mutants exhibiting proximal mitosis in the germ line. At the meeting, we will present preliminary phenotypic analysis and genetic data from selected mutants in this phenotypic class.

CL2179

Caenorhabditis elegans

CL2337

Caenorhabditis elegans

Barnes TM et al. (1995) Worm Breeder's Gazette "arf, arf, arf! A dogged tale."

Hekimi S, Barnes TM

[Worm Breeder's Gazette, 1995]

Just downstream of the unc-24 gene on IV is a gene with profound similarity to vertebrate and invertebrate ADP-ribosylation factors, as revealed by our genomic DNA sequencing. Two other such genes have previously been reported (Murtagh et al. WM 91), called arf-1 III and arf-2 II. We propose naming the gene downstream of unc-24 arf-3. ARF proteins are N-myristoylated GTPases which move from the cytosol to the membrane upon GTP binding, and are involved in vesicular budding in intra-Golgi and ER - Golgi transport. ARF proteins also activate an isoform of phospholipase D, and their crystal structure is known. They were originally named for their ability to act as cofactors in the ADP-ribosylation of Gsa by cholera toxin, an activity whose relationship to the foregoing is not well understood. There is another family of proteins very similar to ARF proteins, but which lack the ability to stimulate ADP ribosylation by cholera toxin and have little effect on phospholipase D, and these have been dubbed ARL proteins, for ARF-like. Within the ARF family, three subtypes have been distinguished on the basis of similarity, namely classes I, II and III. ARLs appear to be a little more diverse, with at least 4 subtypes. ARFs are more similar to each other (80-97% identity) than ARLs are to each other (30-75% identity) and there is even less similarity across groups (35-55% identity). A search of the emerging genomic DNA sequence of chromosomes II, III and X reveals 4 new ARLs, as defined by sequence similarity. However, this analysis also suggests that arf-2 (Murtagh et al. WM 91) is, in fact, an ARL (most closely related to ARL2), not an ARF. That is, there are 2 ARFs (arf-1 and arf-3) and 5 ARLs (arf-2, arl-1 III (C38D4.8), arl-2 III (ZK632.8), arl-3 II (F54C9; like ARL1) and arl-4 II (ZK1320)). By similarity, arf-1 is class I, and arf-3 is class II. Therefore arf-2 has been renamed arl-5 (J. Hodgkin, pc).