scholarly journals Mutations in the bli-4 (I) locus of Caenorhabditis elegans disrupt both adult cuticle and early larval development.

Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 95-102 ◽  
Author(s):  
K Peters ◽  
J McDowall ◽  
A M Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Adult Stage ◽  
Null Alleles ◽  
Recessive Mutation ◽  
Complex Locus ◽  
In Trans ◽  
Essential Function ◽  
Early Larval Development ◽  
I Gene ◽  
New Alleles

Abstract The bli-4 (I) gene of Caenorhabditis elegans had been previously defined by a single recessive mutation, e937, which disrupts the structure of adult-stage cuticle causing the formation of fluid-filled separations of the cuticle layers, or blisters. We report the identification of 11 new alleles of bli-4, all early larval lethals, including an allele induced by transposon mutagenesis. Nine of the lethal alleles failed to complement the blistered phenotype of e937; two alleles, s90 and h754, complement e937. The complementing alleles arrested development somewhat later than the noncomplementing alleles, which blocked just prior to hatching. We conclude that bli-4 is a complex locus with an essential function late in embryogenesis. We investigated the blistered phenotype of e937 through interactions with other mutations that alter worm morphology or cuticle structure. Recessive and dominant epistasis of several dumpy mutations over the blistered phenotype was observed. Using two heterochronic mutations that alter the developmental stage at which adult cuticle is expressed, we observed that adult worms that lack an adult-stage cuticle could not express blisters. However, late larval worms that expressed the adult cuticle did not express blisters either. It seems likely that the presence of the adult cuticle is necessary, but not sufficient, for blister expression. Blistering resulting from e937 is more severe in trans to null alleles, indicating that e937 is hypomorphic. We postulate that the adult-specific blistering is due to an altered or reduced function of bli-4 gene product in the adult cuticle.(ABSTRACT TRUNCATED AT 250 WORDS)

ISOLATION AND GENETIC CHARACTERIZATION OF CELL-LINEAGE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 435-454 ◽  
Author(s):  
H Robert Horvitz ◽  
John E Sulston
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
Null Alleles ◽  
Recessive Mutation ◽  
Incomplete Penetrance ◽  
Nematode Caenorhabditis Elegans ◽  
Cell Lineages ◽  
Cell Divisions ◽  
Recessive Mutations

ABSTRACT Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.

scholarly journals GENE INTERACTIONS AFFECTING MUSCLE ORGANIZATION IN CAENORHABDITIS ELEGANS

Genetics ◽  
1985 ◽  
Vol 110 (3) ◽  
pp. 421-440
Author(s):  
Susan J Brown ◽  
Donald L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Direct Effect ◽  
Double Mutant ◽  
Suppressor Gene ◽  
Null Alleles ◽  
Gene Interactions ◽  
Wild Type ◽  
Recessive Mutations ◽  
New Gene ◽  
New Alleles

ABSTRACT Revertants of unc-15(e73)I, a paralyzed mutant with an altered muscle paramyosin, include six dominant and two recessive intragenic unc-15 revertants, two new alleles of the previously identified suppressor gene, sup-3 V, and a new suppressor designated sup-19(m210)V. The recessive intragenic unc-15 revertants exhibit novel alterations in paramyosin paracrystal structure and distribution, and these alterations are modified by interaction with unc-82(e1220)IV, another mutation that affects paramyosin. A strain containing both unc-15 and a mutation in sup-3 V that restores movement was mutagenized, and paralyzed mutants resembling unc-15 were isolated. Twenty mutations that interfere with suppression were divided into three classes (nonmuscle, sus-1, and mutations within sup-3) based on phenotype, genetic map position and dominance. The nonmuscle mutations include dumpy and uncoordinated types that have no obvious direct effect on muscle organization. Two recessive mutations define a new gene, sus-1 III. These mutations modify the unc-15(e73) phenotype to produce a severely paralyzed, dystrophic double mutant that is not suppressed by sup-3. Five semidominant, intragenic sup-3 antisuppressor mutations, one of which occurred spontaneously, restore the wild-type sup-3 phenotype of nonsuppression. However, reversion of these mutants generated no new suppressor alleles of sup-3, suggesting that the sup-3 antisuppressor alleles are not wild type but may be null alleles.

Genetic studies of mei-1 gene activity during the transition from meiosis to mitosis in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 199-210 ◽  
Author(s):  
T R Clandinin ◽  
P E Mains
Keyword(s):  
Caenorhabditis Elegans ◽  
Null Alleles ◽  
Mitotic Spindles ◽  
Dominant Effect ◽  
Genetic Studies ◽  
In Trans ◽  
In Cis ◽  
Normal Meiosis

Abstract Genetic evidence suggests that the mei-1 locus of Caenorhabditis elegans encodes a maternal product required for female meiosis. However, a dominant gain-of-function allele, mei-1(ct46), can support normal meiosis but causes defects in subsequent mitotic spindles. Previously identified intragenic suppressors of ct46 lack functional mei-1 activity; null alleles suppress only in cis but other alleles arise frequently and suppress both in cis and in trans. Using a different screen for suppressors of the dominant ct46 defect, the present study describes another type of intragenic mutation that also arises at high frequency. These latter alleles appear to have reduced meiotic activity and retain a weakened dominant effect. Characterization of these alleles in trans-heterozygous combinations with previously identified mei-1 alleles has enabled us to define more clearly the role of the mei-1 gene product during normal embryogenesis. We propose that a certain level of mei-1 activity is required for meiosis but must be eliminated prior to mitosis. The dominant mutation causes mei-1 activity to function at mitosis; intragenic trans-suppressors act in an antimorphic manner to inactivate multimeric mei-1 complexes. We propose that inactivation of meiosis-specific functions may be an essential precondition of mitosis; failure to eliminate such functions may allow ectopic meiotic activity during mitosis and cause embryonic lethality.

scholarly journals The Drosophila mei-S332 gene promotes sister-chromatid cohesion in meiosis following kinetochore differentiation.

Genetics ◽  
1992 ◽  
Vol 130 (4) ◽  
pp. 827-841 ◽  
Author(s):  
A W Kerrebrock ◽  
W Y Miyazaki ◽  
D Birnby ◽  
T L Orr-Weaver
Keyword(s):  
Sister Chromatid ◽  
Late Onset ◽  
Sister Chromatid Cohesion ◽  
Null Alleles ◽  
Sister Chromatids ◽  
Late Anaphase ◽  
Chromatid Cohesion ◽  
In Trans ◽  
New Alleles ◽  
Meiosis I

Abstract The Drosophila mei-S332 gene acts to maintain sister-chromatid cohesion before anaphase II of meiosis in both males and females. By isolating and analyzing seven new alleles and a deficiency uncovering the mei-S332 gene we have demonstrated that the onset of the requirement for mei-S332 is not until late anaphase I. All of our alleles result primarily in equational (meiosis II) nondisjunction with low amounts of reductional (meiosis I) nondisjunction. Cytological analysis revealed that sister chromatids frequently separate in late anaphase I in these mutants. Since the sister chromatids remain associated until late in the first division, chromosomes segregate normally during meiosis I, and the genetic consequences of premature sister-chromatid dissociation are seen as nondisjunction in meiosis II. The late onset of mei-S332 action demonstrated by the mutations was not a consequence of residual gene function because two strong, and possibly null, alleles give predominantly equational nondisjunction both as homozygotes and in trans to a deficiency. mei-S332 is not required until after metaphase I, when the kinetochore differentiates from a single hemispherical kinetochore jointly organized by the sister chromatids into two distinct sister kinetochores. Therefore, we propose that the mei-S322 product acts to hold the doubled kinetochore together until anaphase II. All of the alleles are fully viable when in trans to a deficiency, thus mei-S332 is not essential for mitosis. Four of the alleles show an unexpected sex specificity.

Isolation of new alleles of the swine TLR4 gene and analysis of its genetic variation

2011 ◽  
Vol 33 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Zhang-Yuan PAN ◽  
Lan YE ◽  
Jing ZHU ◽  
Zi-Dong DU ◽  
Xiao-Guo HUANG ◽  
...  
Keyword(s):  
Genetic Variation ◽  
I Gene ◽  
New Alleles

Genetic analysis of oxygen defense mechanisms in Drosophila melanogaster and identification of a novel behavioural mutant with a Shaker phenotype

Genome ◽  
1996 ◽  
Vol 39 (4) ◽  
pp. 749-757 ◽  
Author(s):  
James M. Humphreys ◽  
Brenda Duyf ◽  
Mei-Ling A. Joiner ◽  
John P. Phillips ◽  
Arthur J. Hilliker
Keyword(s):  
Drosophila Melanogaster ◽  
Defense Mechanisms ◽  
Chromosome Region ◽  
Recessive Mutation ◽  
Ether Anaesthesia ◽  
Ros Metabolism ◽  
Chromosome Mutations ◽  
New Gene ◽  
New Alleles

Mutants of Drosophila melanogaster that lack Cu/Zn superoxide dismutase or urate are hypersensitive to reactive oxygen species (ROS) generated in vivo by the redox-cycling agent paraquat. We have subsequently employed paraquat as a selective agent to identify adult viable mutants potentially defective in other, perhaps unknown, components of ROS metabolism. Paraquat screening of ethyl methanesulfonate-induced second- and third-chromosome mutations yielded 24 paraquat hypersensitive mutants. Two mutants were identified as being new alleles of the previously identified doublesex (dsx) and pink (p) genes. The remainder of the mutations identified previously undescribed genes, including one second chromosome paraquat hypersensitive mutant that was found to exhibit shaking legs, abdomen pulsations, and body shuddering under ether anaesthesia. This recessive mutation was mapped to the polytene chromosome region of 48A5–48B2 and defines a new gene we named quiver (qvr). This mutation is similar in phenotype to the Shaker (Sh), ether-a-gogo (eag), and Hyperkinetic (Hk) mutations, all of which affect potassium channel function in D. melanogaster. Key words : Drosophila, paraquat, EMS-mutagenesis, Shaker, oxidative-stress.

scholarly journals NHR-40, a Caenorhabditis elegans supplementary nuclear receptor, regulates embryonic and early larval development

2006 ◽  
Vol 123 (9) ◽  
pp. 689-701 ◽  
Author(s):  
Eva Brožová ◽  
Kateřina Šimečková ◽  
Zdeněk Kostrouch ◽  
Joseph Edward Rall ◽  
Marta Kostrouchová
Keyword(s):  
Caenorhabditis Elegans ◽  
Larval Development ◽  
Nuclear Receptor ◽  
Early Larval Development

Dominant maternal-effect mutations causing embryonic lethality in Caenorhabditis elegans.

Genetics ◽  
1990 ◽  
Vol 125 (2) ◽  
pp. 351-369 ◽  
Author(s):  
P E Mains ◽  
I A Sulston ◽  
W B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Maternal Effect ◽  
Gene Dosage ◽  
Recessive Mutation ◽  
Dominant Male ◽  
Temperature Sensitive ◽  
Male Mating ◽  
Loss Of Function ◽  
Dominant Mutant ◽  
Embryonic Viability

Abstract We undertook screens for dominant, temperature-sensitive, maternal-effect embryonic-lethal mutations of Caenorhabditis elegans as a way to identify certain classes of genes with early embryonic functions, in particular those that are members of multigene families and those that are required in two copies for normal development. The screens have identified eight mutations, representing six loci. Mutations at three of the loci result in only maternal effects on embryonic viability. Mutations at the remaining three loci cause additional nonmaternal (zygotic) effects, including recessive lethality or sterility and dominant male mating defects. Mutations at five of the loci cause visible pregastrulation defects. Three mutations appear to be allelic with a recessive mutation of let-354. Gene dosage experiments indicate that one mutation may be a loss-of-function allele at a haploin sufficient locus. The other mutations appear to result in gain-of-function "poison" gene products. Most of these become less deleterious as the relative dosage of the corresponding wild-type allele is increased; we show that relative self-progeny viabilities for the relevant hermaphrodite genotypes are generally M/+/+ greater than M/+ greater than M/M/+ greater than M/Df greater than M/M, where M represents the dominant mutant allele.

scholarly journals Site-selected insertion of the transposon Tc1 into a Caenorhabditis elegans myosin light chain gene.

1993 ◽  
Vol 13 (2) ◽  
pp. 902-910 ◽  
Author(s):  
A M Rushforth ◽  
B Saari ◽  
P Anderson
Keyword(s):  
Polymerase Chain Reaction ◽  
Caenorhabditis Elegans ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Null Alleles ◽  
Chain Gene ◽  
Splice Sites ◽  
Chain Reaction ◽  
Light Chain Gene ◽  
Polymerase Chain

We used the polymerase chain reaction to detect insertions of the transposon Tc1 into mlc-2, one of two Caenorhabditis elegans regulatory myosin light chain genes. Our goals were to develop a general method to identify mutations in any sequenced gene and to establish the phenotype of mlc-2 loss-of-function mutants. The sensitivity of the polymerase chain reaction allowed us to identify nematode populations containing rare Tc1 insertions into mcl-2. mlc-2::Tc1 mutants were subsequently isolated from these populations by a sib selection procedure. We isolated three mutants with Tc1 insertions within the mlc-2 third exon and a fourth strain with Tc1 inserted in nearby noncoding DNA. To demonstrate the generality of our procedure, we isolated two additional mutants with Tc1 insertions within hlh-1, the C. elegans MyoD homolog. All of these mutants are essentially wild type when homozygous. Despite the fact that certain of these mutants have Tc1 inserted within exons of the target gene, these mutations may not be true null alleles. All three of the mlc-2 mutants contain mlc-2 mRNA in which all or part of Tc1 is spliced from the pre-mRNA, leaving small in-frame insertions or deletions in the mature message. There is a remarkable plasticity in the sites used to splice Tc1 from these mlc-2 pre-mRNAs; certain splice sites used in the mutants are very different from typical eukaryotic splice sites.

Measurements of Morphology and Locomotion of Caenorhabditis Elegans With Digital Holographic Microscopy

2020 ◽  
Author(s):  
Yijie Wang ◽  
Jun Chen ◽  
Yuan Zhang ◽  
Kee-Hong Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Zebrafish Embryo ◽  
Adult Stage ◽  
Experimental Studies ◽  
Digital Holographic Microscopy ◽  
Development Stages ◽  
C Elegans ◽  
Applied Development ◽  
Time Period ◽  
Holographic Microscopy

Abstract Digital holographic microscopy (DHM) enables 3D volumetric measurements of small objects with high magnification. DHM has been applied to measure a variety of experimental studies, including turbulent boundary layer, spray droplets, individual cells, development of zebrafish embryo, etc. In this study, a DHM system is applied to measure the morphology and locomotion of two groups of Caenorhabditis Elegans (C. Elegans) with different development conditions (ATGL-1 group and n2 group) in an 8-day time period from their hatching to the adult stage, whose body lengths range from hundreds of micrometers to one millimeter. The length and volume are determined to describe the morphology of the C. Elegans at different development stages. The locomotion of the C. Elegans is divided into linear motion and curl motion. The kinetic energy derived from the two types of motion describes the extent of how active the C. Elegans is. The statistics of morphology and locomotion of the two groups of C. Elegans are compared at different development stages to illustrate the influence of the applied development conditions.

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