Mutations in the 8 kDa dynein light chain gene disrupt sensory axon projections in the Drosophila imaginal CNS

Development ◽  
1996 ◽  
Vol 122 (10) ◽  
pp. 2955-2963 ◽  
Author(s):  
R. Phillis ◽  
D. Statton ◽  
P. Caruccio ◽  
R.K. Murphey
Keyword(s):  
Light Chain ◽  
Cytoplasmic Dynein ◽  
Null Alleles ◽  
Chain Gene ◽  
Sensory Axon ◽  
Axon Pathfinding ◽  
Dynein Light Chain ◽  
Light Chain Gene ◽  
Point Of Entry ◽  
Mutant Female

Mutations in an 8 kDa (8x10(3) Mr) cytoplasmic dynein light chain disrupt sensory axon trajectories in the imaginal nervous system of Drosophila. Weak alleles are behaviorally mutant, female-sterile and exhibit bristle thinning and bristle loss. Null alleles are lethal in late pupal stages and alter neuronal anatomy within the imaginal CNS. We utilized P[Gal4] inserts to examine the axon projections of stretch receptor neurons and an engrailed-lacZ construct to characterize the anatomy of tactile neurons. In mutant animals both types of sensory neurons exhibited altered axon trajectories within the CNS, suggesting a defect in axon pathfinding. However, the alterations in axon trajectory did not prevent these axons from reaching their normal termination regions. In the alleles producing these neuronal phenotypes, expression of the cytoplasmic dynein 8 kDa light chain gene is completely absent. These results demonstrate a new function for the cytoplasmic dynein light chain in the regulation of axonogenesis and may provide a point of entry for studies of the role of cellular motors in growth cone guidance.

scholarly journals Cytoplasmic dynein (ddlc1) mutations cause morphogenetic defects and apoptotic cell death in Drosophila melanogaster.

1996 ◽  
Vol 16 (5) ◽  
pp. 1966-1977 ◽  
Author(s):  
T Dick ◽  
K Ray ◽  
H K Salz ◽  
W Chia
Keyword(s):  
Drosophila Melanogaster ◽  
Light Chain ◽  
Blot Analysis ◽  
Cytoplasmic Dynein ◽  
P Element ◽  
Female Sterility ◽  
Dynein Light Chain ◽  
Loss Of Function ◽  
Light Chain Gene

We report the molecular and genetic characterization of the cytoplasmic dynein light-chain gene, ddlc1, from Drosophila melanogaster. ddlc1 encodes the first cytoplasmic dynein light chain identified, and its genetic analysis represents the first in vivo characterization of cytoplasmic dynein function in higher eucaryotes. The ddlc1 gene maps to 4E1-2 and encodes an 89-amino-acid polypeptide with a high similarity to the axonemal 8-kDa outer-arm dynein light chain from Chlamydomonas flagella. Developmental Northern (RNA) blot analysis and ovary and embryo RNA in situ hybridizations indicate that the ddlc1 gene is expressed ubiquitously. Anti-DDLC1 antibody analyses show that the DDLC1 protein is localized in the cytoplasm. P-element-induced partial-loss-of-function mutations cause pleiotropic morphogenetic defects in bristle and wing development, as well as in oogenesis, and hence result in female sterility. The morphological abnormalities found in the ovaries are always associated with a loss of cellular shape and structure, as visualized by a disorganization of the actin cytoskeleton. Total-loss-of-function mutations cause lethality. A large proportion of mutant animals degenerate during embryogenesis, and the dying cells show morphological changes characteristic of apoptosis, namely, cell and nuclear condensation and fragmentation, as well as DNA degradation. Cloning of the human homolog of the ddlc1 gene, hdlc1, demonstrates that the dynein light-chain 1 is highly conserved in flies and humans. Northern blot analysis and epitope tagging show that the hdlc1 gene is ubiquitously expressed and that the human dynein light chain 1 is localized in the cytoplasm. hdlc1 maps to 14q24.

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.

A tomato dynein light chain gene SlLC6D is a negative regulator of chilling stress

Plant Science ◽  
2021 ◽  
Vol 303 ◽  
pp. 110753
Author(s):  
Tixu Hu ◽  
Shufeng Wang ◽  
Qi Wang ◽  
Xin Xu ◽  
Qiqi Wang ◽  
...  
Keyword(s):  
Light Chain ◽  
Chilling Stress ◽  
Negative Regulator ◽  
Chain Gene ◽  
Dynein Light Chain ◽  
Light Chain Gene

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.

Cloning and characterization of a dynein light chain gene from Puccinia striiformis f. sp. tritici

2014 ◽  
Vol 54 (S1) ◽  
pp. S32-S41
Author(s):  
Jie Liu ◽  
Qiong Zhang ◽  
Qing Chang ◽  
Qiuling Wang ◽  
Lina Han ◽  
...  
Keyword(s):  
Light Chain ◽  
Puccinia Striiformis ◽  
Chain Gene ◽  
Dynein Light Chain ◽  
Light Chain Gene

scholarly journals Disruption of the murine dynein light chain gene Tcte3-3 results in asthenozoospermia

Reproduction ◽  
2010 ◽  
Vol 139 (1) ◽  
pp. 99-111 ◽  
Author(s):  
Sajid Rashid ◽  
Pawel Grzmil ◽  
Joerg-Detlef Drenckhahn ◽  
Andreas Meinhardt ◽  
Ibrahim Adham ◽  
...  
Keyword(s):  
Germ Cell ◽  
Sperm Motility ◽  
Light Chain ◽  
Male Germ Cell ◽  
Chain Gene ◽  
Dynein Light Chain ◽  
Flagellar Motility ◽  
Light Chain Gene ◽  
Germ Cell Differentiation

To elucidate the role of the mouse geneTcte3(Tctex2), which encodes a putative light chain of the outer dynein arm of cilia and sperm flagella, we have inactivated this gene in mice using targeted disruption. Breeding of heterozygous males and females resulted in normal litter size; however, we were not able to detect homozygousTcte3-deficent mice using standard genotype techniques. In fact, our results indicate the presence of at least three highly similar copies of theTcte3gene (Tcte3-1,Tcte3-2, andTcte3-3) in the murine genome. Therefore, quantitative real-time PCR was established to differentiate between mice having one or two targetedTcte3-3alleles. By this approach,Tcte3-3−/−animals were identified, which were viable and revealed no obvious malformation. Interestingly, some homozygousTcte3-3-deficient male mice bred with wild-type female produced no offspring while otherTcte3-3-deficient males revealed decreased sperm motility but were fertile. In infertileTcte3-3−/−males, spermatogenesis was affected and sperm motility was reduced, too, resulting in decreased ability of Tcte3-3-deficient spermatozoa to move from the uterus into the oviduct. Impaired flagellar motility is not correlated with any gross defects in the axonemal structure, since outer dynein arms are detectable in sperm ofTcte3-3−/−males. However, in infertile males, deficientTcte3-3function is correlated with increased apoptosis during male germ cell development, resulting in a reduction of sperm number. Moreover, multiple malformations in developing haploid germ cells are present. Our results support a role ofTcte3-3in generation of sperm motility as well as in male germ cell differentiation.

Sign in / Sign up

Export Citation Format

Share Document