scholarly journals Isolation and Characterization of pmk-(1–3): Three p38 Homologs in Caenorhabditis elegans

2001 ◽  
Vol 4 (6) ◽  
pp. 337-344 ◽  
Author(s):  
Kevin Berman ◽  
Jim McKay ◽  
Leon Avery ◽  
Melanie Cobb
Keyword(s):  
Caenorhabditis Elegans ◽  
Isolation And Characterization

Fragile skeletal muscle attachments in dystrophic mutants of Caenorhabditis elegans: isolation and characterization of the mua genes

Development ◽  
2000 ◽  
Vol 127 (6) ◽  
pp. 1197-1207 ◽  
Author(s):  
J.D. Plenefisch ◽  
X. Zhu ◽  
E.M. Hedgecock
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Wall ◽  
Local Strain ◽  
Muscle Differentiation ◽  
The Body ◽  
Tissue Separation ◽  
New Genes ◽  
Isolation And Characterization ◽  
Skin Fragility

Over 30 Caenorhabditis elegans mutants were identified with normal muscle differentiation and initial locomotion followed by catastrophic detachment of skeletal muscles from the body wall. Reducing the strength of muscle contraction in these mutants with a myosin gene mutation suppresses muscle detachment. These dystrophic mutants identify a novel class of genes required for growth and maintenance of functional muscle attachments, not exceptional alleles of genes required for muscle differentiation and contractility. Nine new genes, named mua, and two previously published loci, unc-23 and vab-10, cause fragile musscle attachments. The primary sites of muscle detachment, including the plane of tissue separation, are characteristic for each gene. We suggest these genes identify feedback mechanisms whereby local strain regulates the extent of myofibril contraction and the placement of new muscle attachments in functioning muscles. Finally, we draw some comparisons to vertebrate skin fragility diseases and muscular dystrophies.

scholarly journals fog-2, a germ-line-specific sex determination gene required for hermaphrodite spermatogenesis in Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 43-61 ◽  
Author(s):  
T Schedl ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Germ Line ◽  
Negative Regulator ◽  
Loss Of Function ◽  
Wild Type ◽  
Negative Regulators ◽  
Nematode Caenorhabditis Elegans ◽  
Isolation And Characterization

Abstract This paper describes the isolation and characterization of 16 mutations in the germ-line sex determination gene fog-2 (fog for feminization of the germ line). In the nematode Caenorhabditis elegans there are normally two sexes, self-fertilizing hermaphrodites (XX) and males (XO). Wild-type XX animals are hermaphrodite in the germ line (spermatogenesis followed by oogenesis), and female in the soma. fog-2 loss-of-function mutations transform XX animals into females while XO animals are unaffected. Thus, wild-type fog-2 is necessary for spermatogenesis in hermaphrodites but not males. The fem genes and fog-1 are each essential for specification of spermatogenesis in both XX and XO animals. fog-2 acts as a positive regulator of the fem genes and fog-1. The tra-2 and tra-3 genes act as negative regulators of the fem genes and fog-1 to allow oogenesis. Two models are discussed for how fog-2 might positively regulate the fem genes and fog-1 to permit spermatogenesis; fog-2 may act as a negative regulator of tra-2 and tra-3, or fog-2 may act positively on the fem genes and fog-1 rendering them insensitive to the negative action of tra-2 and tra-3.

scholarly journals CHARACTERIZATION OF TEMPERATURE-SENSITIVE, FERTILIZATION-DEFECTIVE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1978 ◽  
Vol 88 (2) ◽  
pp. 285-303 ◽  
Author(s):  
Samuel Ward ◽  
Johji Miwa
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Wild Type ◽  
Normal Numbers ◽  
Primary Defect ◽  
Isolation And Characterization ◽  
Pass Through

ABSTRACT The isolation and characterization of three Caenorhabditis elegans temperature-sensitive mutants that are defective at fertilization are described. All three are alleles of the gene fer-1. At the restrictive temperature of 25°, mutant hermaphrodites make sperm and oocytes in normal numbers. No oocytes are fertilized, although they pass through the spermatheca and uterus normally. The oocytes can be fertilized by sperm transferred by wild-type males, indicating that the mutant defect is in the sperm. The temperature-sensitive period for the mutants coincides with spermatogenesis. Sperm made by mutants at 25° cannot be distinguished from wild-type sperm by light microscopy. The sperm do contact oocytes in mutant hermaphrodites, but do not fertilize. Mutant sperm appear to be nonmotile. Mutant males are also sterile when grown at 25°. They transfer normal numbers of sperm to hermaphrodites at mating, but these sperm fail to migrate to the spermatheca and are infertile. The phenotype of these mutants is consistent with a primary defect in sperm motility, but the cause of this defect is not known.

scholarly journals New Genes That Interact With lin-35 Rb to Negatively Regulate the let-60 ras Pathway in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 164 (1) ◽  
pp. 135-151 ◽  
Author(s):  
Jeffrey H Thomas ◽  
Craig J Ceol ◽  
Hillel T Schwartz ◽  
H Robert Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Intercellular Signaling ◽  
Ras Pathway ◽  
Class A ◽  
New Genes ◽  
Isolation And Characterization ◽  
Vulval Precursor Cells ◽  
Class B ◽  
In The Wild

Abstract Previous studies have shown that a synthetic multivulva phenotype results from mutations in genes that antagonize the ras-mediated intercellular signaling system responsible for vulval induction in Caenorhabditis elegans. Synthetic multivulva mutations define two classes of genes, A and B, and a mutation in a gene of each class is required to produce the multivulva phenotype. The ectopic vulval tissue in multivulva animals is generated by vulval precursor cells that in the wild type do not generate vulval tissue. One of the class B synthetic multivulva genes, lin-35, encodes a protein similar to the retinoblastoma (Rb) protein. In this article, we describe the isolation and characterization of 50 synthetic multivulva mutations, the identification of new components of both the class A and class B lin-35 Rb pathways, and the cloning of lin-52, a class B gene that may have a conserved role in Rb-mediated signaling.

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