scholarly journals Dominant unc-37 mutations suppress the movement defect of a homeodomain mutation in unc-4, a neural specificity gene in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 741-753 ◽  
Author(s):  
D M Miller ◽  
C J Niemeyer ◽  
P Chitkara
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Synaptic Input ◽  
Neuronal Morphology ◽  
Axonal Guidance ◽  
Temperature Sensitive ◽  
Homeodomain Protein ◽  
Loss Of Function ◽  
Selection Scheme ◽  
Synaptic Specificity

Abstract The unc-4 gene of Caenorhabditis elegans encodes a homeodomain protein that defines synaptic input to ventral cord motor neurons. unc-4 mutants are unable to crawl backward because VA motor neurons are miswired with synaptic connections normally reserved for their sister cells, the VB motor neurons. These changes in connectivity are not accompanied by any visible effects upon neuronal morphology, which suggests that unc-4 regulates synaptic specificity but not axonal guidance or outgrowth. In an effort to identify other genes in the unc-4 pathway, we have devised a selection scheme for rare mutations that suppress the Unc-4 phenotype. We have isolated four, dominant, extragenic, allele-specific suppressors of unc-4(e2322ts), a temperature sensitive allele with a point mutation in the unc-4 homeodomain. Our data indicate that these suppressors are gain-of-function mutations in the previously identified unc-37 gene. We show that the loss-of-function mutation unc-37(e262) phenocopies the Unc-4 movement defect but does not prevent unc-4 expression or alter VA motor neuron morphology. These findings suggest that unc-37 functions with unc-4 to specify synaptic input to the VA motor neurons. We propose that unc-37 may be regulated by unc-4. Alternatively, unc-37 may encode a gene product that interacts with the unc-4 homeodomain.

C. elegans unc-4 gene encodes a homeodomain protein that determines the pattern of synaptic input to specific motor neurons

Nature ◽  
1992 ◽  
Vol 355 (6363) ◽  
pp. 841-845 ◽  
Author(s):  
David M. Miller ◽  
Michael M. Shen ◽  
Caroline E. Shamu ◽  
Thomas R. Bürglin ◽  
Gary Ruvkun ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Synaptic Input ◽  
Homeodomain Protein ◽  
C Elegans

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.

Patterning of dopaminergic neurotransmitter identity among Caenorhabditis elegans ray sensory neurons by a TGFbeta family signaling pathway and a Hox gene

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5819-5831 ◽  
Author(s):  
R. Lints ◽  
S.W. Emmons
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Signaling Pathway ◽  
Cell Fate ◽  
Sensory Neurons ◽  
Ectopic Expression ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Hox Gene

We have investigated the mechanism that patterns dopamine expression among Caenorhabditis elegans male ray sensory neurons. Dopamine is expressed by the A-type sensory neurons in three out of the nine pairs of rays. We used expression of a tyrosine hydroxylase reporter transgene as well as direct assays for dopamine to study the genetic requirements for adoption of the dopaminergic cell fate. In loss-of-function mutants affecting a TGFbeta family signaling pathway, the DBL-1 pathway, dopaminergic identity is adopted irregularly by a wider subset of the rays. Ectopic expression of the pathway ligand, DBL-1, from a heat-shock-driven transgene results in adoption of dopaminergic identity by rays 3–9; rays 1 and 2 are refractory. The rays are therefore prepatterned with respect to their competence to be induced by a DBL-1 pathway signal. Temperature-shift experiments with a temperature-sensitive type II receptor mutant, as well as heat-shock induction experiments, show that the DBL-1 pathway acts during an interval that extends from two to one cell generation before ray neurons are born and begin to differentiate. In a mutant of the AbdominalB class Hox gene egl-5, rays that normally express EGL-5 do not adopt dopaminergic fate and cannot be induced to express DA when DBL-1 is provided by a heat-shock-driven dbl-1 transgene. Therefore, egl-5 is required for making a subset of rays capable of adopting dopaminergic identity, while the function of the DBL-1 pathway signal is to pattern the realization of this capability.

Control of hindbrain motor neuron differentiation by the homeobox gene Phox2b

Development ◽  
2000 ◽  
Vol 127 (7) ◽  
pp. 1349-1358 ◽  
Author(s):  
A. Pattyn ◽  
M. Hirsch ◽  
C. Goridis ◽  
J.F. Brunet
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Early Stage ◽  
Control Point ◽  
Homeobox Gene ◽  
Homeodomain Protein ◽  
Loss Of Function ◽  
Dorsoventral Patterning ◽  
Cns Neurons ◽  
Mantle Layer

Motor neurons are a widely studied model of vertebrate neurogenesis. They can be subdivided in somatic, branchial and visceral motor neurons. Recent studies on the dorsoventral patterning of the rhombencephalon have implicated the homeobox genes Pax6 and Nkx2.2 in the early divergence of the transcriptional programme of hindbrain somatic and visceral motor neuronal differentiation. We provide genetic evidence that the paired-like homeodomain protein Phox2b is required for the formation of all branchial and visceral, but not somatic, motor neurons in the hindbrain. In mice lacking Phox2b, both the generic and subtype-specific programs of motoneuronal differentiation are disrupted at an early stage. Most motor neuron precursors die inside the neuroepithelium while those that emigrate to the mantle layer fail to switch on early postmitotic markers and to downregulate neuroepithelial markers. Thus, the loss of function of Phox2b in hindbrain motor neurons exemplifies a novel control point in the generation of CNS neurons.

scholarly journals Caenorhabditis elegans mutants defective in the functioning of the motor neurons responsible for egg laying.

Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 703-721 ◽  
Author(s):  
C Desai ◽  
H R Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Synaptic Transmission ◽  
Motor Neurons ◽  
Egg Laying ◽  
The Other ◽  
Single Type ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Sensitive Allele

Abstract We have isolated and characterized 45 Caenorhabditis elegans mutants presumed to be defective in the functioning of the hermaphrodite-specific neurons (HSNs). Like hermaphrodites that lack the HSN motor neurons, these mutants are egg-laying defective and do not lay eggs in response to exogenous imipramine but do lay eggs in response to exogenous serotonin. Twenty of the 45 mutations define 10 new egl genes; the other 25 mutations are alleles of five previously defined genes, four of which are known to affect the HSNs. Seven mutations in three genes cause the HSNs to die in hermaphrodites, as they normally do in males. These genes appear to be involved in the determination of the sexual phenotype of the HSNs, and one of them (egl-41) is a newly identified gene that may function generally in sex determination. Five of the 15 genes are defined only by mutations that have dominant effects on egg laying. One gene egl(n1108), is defined by a temperature-sensitive allele that has a temperature-sensitive period after HSN development is complete, suggesting that egl(n1108) may be involved in HSN synaptic transmission. Four of the genes are defined by single alleles, which suggests that other such genes remain to be discovered. Mutations in no more than 4 of the 15 genes specifically affect the HSNs, indicating that there are few genes with functions needed only in this single type of nerve cell.

scholarly journals Analysis of the role of tra-1 in germline sex determination in the nematode Caenorhabditis elegans.

Genetics ◽  
1989 ◽  
Vol 123 (4) ◽  
pp. 755-769 ◽  
Author(s):  
T Schedl ◽  
P L Graham ◽  
M K Barton ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Germ Line ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Wild Type ◽  
Allelic Series ◽  
Isolation And Characterization ◽  
Somatic Gonad

Abstract In wild-type Caenorhabditis elegans there are two sexes, self-fertilizing hermaphrodites (XX) and males (XO). To investigate the role of tra-1 in controlling sex determination in germline tissue, we have examined germline phenotypes of nine tra-1 loss-of-function (lf) mutations. Previous work has shown that tra-1 is needed for female somatic development as the nongonadal soma of tra-1(lf) XX mutants is masculinized. In contrast, the germline of tra-1(lf) XX and XO animals is often feminized; a brief period of spermatogenesis is followed by oogenesis, rather than the continuous spermatogenesis observed in wild-type males. In addition, abnormal gonadal (germ line and somatic gonad) phenotypes are observed which may reflect defects in development or function of somatic gonad regulatory cells. Analysis of germline feminization and abnormal gonadal phenotypes of the various mutations alone or in trans to a deficiency reveals that they cannot be ordered in an allelic series and they do not converge to a single phenotypic endpoint. These observations lead to the suggestion that tra-1 may produce multiple products and/or is autoregulated. One interpretation of the germline feminization is that tra-1(+) is necessary for continued specification of spermatogenesis in males. We also report the isolation and characterization of tra-1 gain-of-function (gf) mutations with novel phenotypes. These include temperature sensitive, recessive germline feminization, and partial somatic loss-of-function phenotypes.

Cell interactions control the direction of outgrowth, branching and fasciculation of the HSN axons of Caenorhabditis elegans

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 1071-1087 ◽  
Author(s):  
G. Garriga ◽  
C. Desai ◽  
H.R. Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Epithelial Cells ◽  
Motor Neurons ◽  
Growth Cone ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Egg Laying ◽  
Axonal Guidance ◽  
Nematode Caenorhabditis Elegans ◽  
Vulval Precursor Cells

The two serotonergic HSN motor neurons of the nematode Caenorhabditis elegans innervate the vulval muscles and stimulate egg laying by hermaphrodites. By analyzing mutant and laser-operated animals, we find that both epithelial cells of the developing vulva and axons of the ventral nerve cord are required for HSN axonal guidance. Vulval precursor cells help guide the growth cone of the emerging HSN axon to the ventral nerve cord. Vulval cells also cause the two HSN axons to join the ventral nerve cord in two separate fascicles and to defasciculate from the ventral nerve cord and branch at the vulva. The axons of either the PVP or PVQ neurons are also necessary for the HSN axons to run in two separate fascicles within the ventral nerve cord. Our observations indicate that the outgrowth of the HSN axon is controlled in multiple ways by both neuronal and nonneuronal cells.

A Limited Number of Caenorhabditis elegans Genes Are Readily Mutable to Dominant, Temperature-Sensitive Maternal-Effect Embryonic Lethality

Genetics ◽  
1997 ◽  
Vol 147 (4) ◽  
pp. 1665-1674 ◽  
Author(s):  
Nancy L Mitenko ◽  
James R Eisner ◽  
John R Swiston ◽  
Paul E Mains
Keyword(s):  
Caenorhabditis Elegans ◽  
Maternal Effect ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Gain Of Function ◽  
C Elegans ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
Dominant Temperature Sensitive

Abstract Dominant gain-of-function mutations can give unique insights into the study of gene function. In addition, gain-of-function mutations, unlike loss-of-function alleles, are not biased against the identification of genetically redundant loci. To identify novel genetic functions active during Caenorhabditis elegans embryogenesis, we have collected a set of dominant temperature-sensitive maternal-effect embryonic lethal mutations. In a previous screen, we isolated eight such mutations, distributed among six genes. In the present study, we describe eight new dominant mutations that identify only three additional genes, yielding a total of 16 dominant mutations found in nine genes. Therefore, it appears that a limited number of C. elegans genes mutate to this phenotype at appreciable frequencies. Five of the genes that we identified by dominant mutations have loss-of-function alleles. Two of these genes may lack loss-of-function phenotypes, indicating that they are nonessential and so may represent redundant loci. Loss-of-function mutations of three other genes are associated with recessive lethality, indicating nonredundancy.

Mutations in the Caenorhabditis elegans unc–4 gene alter the synaptic input to ventral cord motor neurons

Nature ◽  
1992 ◽  
Vol 355 (6363) ◽  
pp. 838-841 ◽  
Author(s):  
J. G. White ◽  
E. Southgate ◽  
J. N. Thomson
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Synaptic Input ◽  
Ventral Cord
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