Mosaic analysis of the let-23 gene function in vulval induction of Caenorhabditis elegans

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2655-2666 ◽  
Author(s):  
M. Koga ◽  
Y. Ohshima
Keyword(s):  
Caenorhabditis Elegans ◽  
Gene Function ◽  
Larval Survival ◽  
Precursor Cell ◽  
Kinase Gene ◽  
Genetic Mosaic ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene ◽  
Almost All ◽  
Vulval Precursor Cell

The let-23 receptor tyrosine kinase gene is required for vulval induction and larval survival in the nematode Caenorhabditis elegans. We carried out genetic mosaic analyses of the let-23 gene function by using the cloned let-23 and ncl-1 genes. The wild-type let-23 gene was required in a vulval precursor cell to adopt the 1 degree vulval fate in animals carrying a let-23 vulvaless or lethal chromosomal mutation. In almost all the animals, vulval precursor cells adjacent to a 1 degree fate cell were induced to the 2 degrees vulval fate regardless of the let-23 genotypes. These findings indicate that the vulval induction signal from an anchor cell induces a vulval precursor cell to adopt the 1 degree fate through LET-23, and then a 1 degree fate cell induces adjacent cells to adopt the 2 degrees fate, for which LET-23 is not required. Foci of lethality of the let-23 (mn23) mutation were found in ABal and ABplp lineages.

scholarly journals Multiple functions of let-23, a Caenorhabditis elegans receptor tyrosine kinase gene required for vulval induction.

Genetics ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 251-267 ◽  
Author(s):  
R V Aroian ◽  
P W Sternberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Egf Receptor ◽  
Kinase Gene ◽  
Multiple Functions ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene ◽  
Epidermal Growth ◽  
Mutant Phenotypes

Abstract The let-23 gene, which encodes a putative tyrosine kinase of the epidermal growth factor (EGF) receptor subfamily, has multiple functions during Caenorhabditis elegans development. We show that let-23 function is required for vulval precursor cells (VPCs) to respond to the signal that induces vulval differentiation: a complete loss of let-23 function results in no induction. However, some let-23 mutations that genetically reduce but do not eliminate let-23 function result in VPCs apparently hypersensitive to inductive signal: as many as five of six VPCs can adopt vulval fates, in contrast to the three that normally do. These results suggest that the let-23 receptor tyrosine kinase controls two opposing pathways, one that stimulates vulval differentiation and another that negatively regulates vulval differentiation. Furthermore, analysis of 16 new let-23 mutations indicates that the let-23 kinase functions in at least five tissues. Since various let-23 mutant phenotypes can be obtained independently, the let-23 gene is likely to have tissue-specific functions.

scholarly journals Splicing in Caenorhabditis elegans does not require an AG at the 3' splice acceptor site.

1993 ◽  
Vol 13 (1) ◽  
pp. 626-637 ◽  
Author(s):  
R V Aroian ◽  
A D Levy ◽  
M Koga ◽  
Y Ohshima ◽  
J M Kramer ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Splice Site ◽  
Splice Acceptor Site ◽  
Acceptor Site ◽  
Kinase Gene ◽  
C Elegans ◽  
Branch Point Sequence ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene

The dinucleotide AG, found at the 3' end of virtually all eukaryotic pre-mRNA introns, is thought to be essential for splicing. Reduction-of-function mutations in two Caenorhabditis elegans genes, the receptor tyrosine kinase gene let-23 and the collagen gene dpy-10, both alter the AG at the end of a short (ca. 50-nucleotide) intron to AA. The in vivo effects of these mutations were studied by sequencing polymerase chain reaction-amplified reverse-transcribed RNA isolated from the two mutants. As expected, we find transcripts that splice to a cryptic AG, skip an exon, and retain an unspliced intron. However, we also find significant levels of splicing at the mutated 3' splice site (AA) and at nearby non-AG dinucleotides. Our results indicate that for short C. elegans introns an AG is not required for splicing at either the correct 3' splice site or incorrect sites. Analysis of a splice site mutant involving a longer, 316-nucleotide C. elegans intron indicates that an AG is also not required there for splicing. We hypothesize that elements besides the invariant AG, e.g., an A-U-rich region, a UUUC motif, and/or a potential branch point sequence, are directing the selection of the 3' splice site and that in wild-type genes these elements cooperate so that proper splicing occurs.

scholarly journals Splicing in Caenorhabditis elegans does not require an AG at the 3' splice acceptor site

1993 ◽  
Vol 13 (1) ◽  
pp. 626-637
Author(s):  
R V Aroian ◽  
A D Levy ◽  
M Koga ◽  
Y Ohshima ◽  
J M Kramer ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Splice Site ◽  
Splice Acceptor Site ◽  
Acceptor Site ◽  
Kinase Gene ◽  
C Elegans ◽  
Branch Point Sequence ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene

The dinucleotide AG, found at the 3' end of virtually all eukaryotic pre-mRNA introns, is thought to be essential for splicing. Reduction-of-function mutations in two Caenorhabditis elegans genes, the receptor tyrosine kinase gene let-23 and the collagen gene dpy-10, both alter the AG at the end of a short (ca. 50-nucleotide) intron to AA. The in vivo effects of these mutations were studied by sequencing polymerase chain reaction-amplified reverse-transcribed RNA isolated from the two mutants. As expected, we find transcripts that splice to a cryptic AG, skip an exon, and retain an unspliced intron. However, we also find significant levels of splicing at the mutated 3' splice site (AA) and at nearby non-AG dinucleotides. Our results indicate that for short C. elegans introns an AG is not required for splicing at either the correct 3' splice site or incorrect sites. Analysis of a splice site mutant involving a longer, 316-nucleotide C. elegans intron indicates that an AG is also not required there for splicing. We hypothesize that elements besides the invariant AG, e.g., an A-U-rich region, a UUUC motif, and/or a potential branch point sequence, are directing the selection of the 3' splice site and that in wild-type genes these elements cooperate so that proper splicing occurs.

scholarly journals Distinct Mutations in the Receptor Tyrosine Kinase Gene ROR2 Cause Brachydactyly Type B

2000 ◽  
Vol 67 (4) ◽  
pp. 822-831 ◽  
Author(s):  
Georg C. Schwabe ◽  
Sigrid Tinschert ◽  
Christian Buschow ◽  
Peter Meinecke ◽  
Gerhard Wolff ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Type B ◽  
Kinase Gene ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene

FLT4 Receptor Tyrosine Kinase Gene Mapping to Chromosome Band 5q35 in Relation to the t(2;5), t(5;6), and t(3;5) Translocations

1993 ◽  
Vol 7 (3) ◽  
pp. 144-151 ◽  
Author(s):  
Elina Armstrong ◽  
Kumar Kastury ◽  
Olga Aprelikova ◽  
Florencia Bullrich ◽  
Christian Nezelof ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Gene Mapping ◽  
Receptor Tyrosine Kinase ◽  
Chromosome Band ◽  
Kinase Gene ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene

scholarly journals The receptor tyrosine kinase gene linotte is required for neuronal pathway selection in the Drosophila mushroom bodies

1998 ◽  
Vol 78 (1-2) ◽  
pp. 47-61 ◽  
Author(s):  
Caroline Moreau-Fauvarque ◽  
Emmanuel Taillebourg ◽  
Elisabeth Boissoneau ◽  
Jacqueline Mesnard ◽  
Jean-Maurice Dura
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Mushroom Bodies ◽  
Kinase Gene ◽  
Neuronal Pathway ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene

Genomic Structure and Promoter Analysis of the Mouse EphA8 Receptor Tyrosine Kinase Gene

2000 ◽  
Vol 19 (5) ◽  
pp. 291-300 ◽  
Author(s):  
Jaemin Jeong ◽  
Sunga Choi ◽  
Changkyu Gu ◽  
Hansoo Lee ◽  
Soochul Park
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Promoter Analysis ◽  
Genomic Structure ◽  
Kinase Gene ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene
Sign in / Sign up

Export Citation Format

Share Document