Burke DJ et al. (1979) Worm Breeder's Gazette "studies on the X-chromosome of Panagrellus redivivus."

Burke DJ, Samoiloff MR, Schulz S

[Worm Breeder's Gazette, 1979]

Mutants on the X-chromosome of the dioecious Panagrellus redivivus have been isolated and mapped. Four uncs and a long have been maintained in both sexes. Paralysed, twitchers and dumpies have been obtained, but males fail to mate. Three of the uncs have reduced mobility or coordination, while the fourth unc contracts when tapped on the head, but will not reverse. The long mutant is approximately 30% longer than wild type, with no decrease in body width, Recently a new phenotype, skinny, more than 100% longer and 25% thinner has been isolated by Yvonne Jordan. The frequency of mutation using standard EMS mutagenesis of L4s is 4. 4 X 10+E-4 mutations per visible locus. The number of essential genes on the P. redivivus X-chromosome is calculated at 320 on the basis of the frequency of lethal mutations corrected for double events. The gamma-irradiation induced mutation rate is 9 X 10+E-7 mutations per locus per rad, using a dose-rate of 4.5 Kr/min. Genetically marked L2s were exposed to doses of gamma radiation varying from 5 to 150 Kr. Using target theory applied to males it was calculated that 180, 130 and 1800 X-linked genes in the total P. redivivus genome are required to complete the second, third and final moult, respectively. The kinetics of the failure of females to develop after gamma-irradiation was more indicitive of chromosome breaks rather than point mutation.

Swanson MM (1982) Worm Breeder's Gazette "CGC Curator's report."

Swanson MM

[Worm Breeder's Gazette, 1982]

Curator's Report: The CGC continues to be a busy place. We have mailed a total of over 800 strains to 51 different labs in 2 and 1/2 years of operation. 390 different strains representing about 46% of our total collection have been mailed upon request. The level of requests continues to increase: 146 strains mailed in year 1, 361 in year 2 and 306 so far this year. The current level is 27% higher than last year. We have a new research technician, Mark Edgley, who is handling most of the strain requests now. The computer information retrieval system is fully operational now and is available for use on request. Rates for use are projected to triple July 1, so we can no longer afford to have the system available at a regularly scheduled time each day. Beginning in September, I will be in Bozeman, Montana for the year. All map data should be mailed to me there in anticipation of the 1983 version of the Genetic Map to be distributed at the next meeting at Cold Spring Harbor. We will send a reminder in December; the deadline will be February 1, 1983. Included here is a new bibliographic update and a list of new strains acquired by the CGC since the last complete strain list was mailed in December. One new lab designation (KR, h) has been assigned to Ann Rose for her new lab at the University of British Columbia Medical School. WANTED: I have heard a rumor that cat-2 and sqt-2 are incorrectly placed on the current map. Anyone with data on these 2 genes please send to me before the next revision.

Hartman PS et al. (1982) Worm Breeder's Gazette "somatic damage to the X chromosome of C elegans induced by gamma radiation."

Hartman PS, Herman RK

[Worm Breeder's Gazette, 1982]

Wild-type males are more sensitive than wild-type hermaphrodites to inactivation by gamma radiation. This sex-specific difference is observed when eggs are irradiated immediately after collection by the hypochlorite method, but it is more pronounced when irradiation is delayed for 22 hours after egg collection. In the latter case, for example, at a dose of 50 kr, survival of males was only about 5% that of hermaphrodites. In both cases, the difference between the inactivation curves of males and hermaphrodites is in the extent of the shoulders and not in the final inactivation slopes. We considered three explanations for this sex-specific difference. First, the difference could be caused by some artifact in scoring the heavily irradiated males and hermaphrodites. Second, the difference could be due to the different sexual phenotypes per se. And third, the difference could be due to the difference in chromosome composition of the two sexes, that is, hermaphrodites are more radiation resistant because they have two X chromosomes rather than one. These possibilities were tested by examining the gamma radiation sensitivities of animals in which the normal correspondence between X chromosome constitution and sexual phenotype was altered by either a her-1 or tra-1 mutation. A her-1 dpy-21 triple mutant was constructed and assayed for radiation sensitivity. The him- 5 mutation insures the constant generation of XO animals; the dpy-21 mutation allows distinction of XO (non-Dpy) versus XX (Dpy) animals; and her-1 transforms XO animals into hermaphrodites. The inactivation curves for non-Dpy (XO) and Dpy (XX) her-1 hermaphrodites were strikingly similar to the curves obtained for wild-type males and hermaphrodites. respectively. Moreover, XX animals transformed into fertile males by a tra-1 mutation did not show increased radiosensitivity relative to their tra-1/dpy-18 sibs. We conclude that the wild-type sex-specific difference is caused by the difference in X chromosome constitution and that inactivation of XO animals by gamma radiation is predominantly due to X-chromosome damage. No sex- specific difference in inactivation was observed after UV irradiation.

Nathoo A et al. (1997) Worm Breeder's Gazette "Putative buccalin-like and myomodulin-like neuropeptides in C. elegans"

Nathoo A, Hart AC

[Worm Breeder's Gazette, 1997]

Neuropeptides form the largest class of neuroactive substances, yet as a group their roles in nervous system function and development are still poorly understood. Only the FMRFamides and related neuropeptides (FaRPs) have been intensely studied in C. elegans. However, in Aplysia californica, over 40 neuropeptides have been identified and characterized. This suggests that many C. elegans neuropeptides have not yet been discovered. With the near completion of the C. elegans genome sequencing project, reverse genetic techniques can be applied to identify C. elegans neuropeptide genes. We are using FASTA and BLAST to search with previously identified neuropeptide sequences (stored in GENBANK) against the C. elegans genome sequence. We expect the products of neuropeptide genes to fit a prepropeptide model: they should contain a putative signal peptide region, followed by interrupted multiple repeats of the same or similar neuropeptide. Additionally, the predicted neuropeptides should be flanked by pairs of basic amino acids (KR, RR, KK, RK) or less frequently by monobasic residues (R or K) which are preferred sites of endoproteolytic cleavage. Potential C. elegans neuropeptide gene compatible with the prepropeptide model are then selected for molecular and genetic analysis. We are currently analyzing C. elegans genes encoding neuropeptides similar to Aplysia buccalin (C. elegans C01C4.1) and myomodulin (C. elegans T24D8.3, T24D8.4, T24D8.5 and T01B6.4). (See below.) Even though the predicted C. elegans neuropeptide sequences are not strikingly similar to the Aplysia neuropeptides, there is strong internal homology between neuropeptides within the same C. elegans genes. We are creating reporter constructs by fusing the promoter region of potential neuropeptide genes to the GFP gene using Fire laboratory vectors. We are injecting these reporter constructs to assess cellular expression patterns of these myomodulin-like and buccalin-like genes. We think that it is likely that the GENEFINDER predicted genes of T24D8.3, .4 and .5 are exons of a single gene. We will use RT-PCR to determine mRNA splicing patterns. Our long range goals include creating mutations in these genes and determining the function of these and other putative C. elegans neuropeptides. Identity is indicated with a colon, gaps with underlining. SLSMLRLG____ Aplysia Myomodulin A :MA:G:::LRPG T24D8.5 :MAYG:Q:FRPG # :IALG:S:FRPG :MAIG:A:MRPG T24D8.4 :IAIG:A:FRPG T24D8.3 N:LVG:Y:FRIG T01B6.4 DPNVDPYSYLPSVG Aplysia Buccalin _VNL::N:FRM:F: C01C4.1 ___M:ANAFRM:F: # ___M::NAFRM:F: