Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans

Makoto Koga, Yasumi Ohshima

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The vulva of the nematode Caenorhabditis elegans develops from the three vulval precursor cells (VPCs) that are induced by a signal from the gonadal anchor cell. This signal is thought to be mediated by a receptor tyrosine kinase (RTK) in the VPCs to a downstream signal transduction pathway. A mitogen-activated protein kinase kinase (MAPKK) has been found to be one of the major components of an RTK pathway in other organisms. We expressed a wild type and an activated cDNA of Dsorl, a Drosophila MAPKK, in each of the three vulvaless mutants lin-3, let-23 and lin-45. The expression of an activated form of Dsorl in each of the mutants effectively induced a normal, functional vulva, that is, suppressed the vulvaless phenotype. The wild type Dsorl also suppressed albeit less effectively. These results suggest that a MAPKK is involved in the vulval induction of C. elegans.

Original languageEnglish
Pages (from-to)15-22
Number of pages8
JournalMechanisms of Development
Volume53
Issue number1
DOIs
Publication statusPublished - Jan 1 1995

Fingerprint

Mitogen-Activated Protein Kinase Kinases
Caenorhabditis elegans
Drosophila
Vulva
Receptor Protein-Tyrosine Kinases
Phenotype
Mutation
Signal Transduction
Complementary DNA

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Embryology
  • Developmental Neuroscience

Cite this

Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans. / Koga, Makoto; Ohshima, Yasumi.

In: Mechanisms of Development, Vol. 53, No. 1, 01.01.1995, p. 15-22.

Research output: Contribution to journalArticle

@article{9d984343bd894345ac6a385dac087a74,
title = "Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans",
abstract = "The vulva of the nematode Caenorhabditis elegans develops from the three vulval precursor cells (VPCs) that are induced by a signal from the gonadal anchor cell. This signal is thought to be mediated by a receptor tyrosine kinase (RTK) in the VPCs to a downstream signal transduction pathway. A mitogen-activated protein kinase kinase (MAPKK) has been found to be one of the major components of an RTK pathway in other organisms. We expressed a wild type and an activated cDNA of Dsorl, a Drosophila MAPKK, in each of the three vulvaless mutants lin-3, let-23 and lin-45. The expression of an activated form of Dsorl in each of the mutants effectively induced a normal, functional vulva, that is, suppressed the vulvaless phenotype. The wild type Dsorl also suppressed albeit less effectively. These results suggest that a MAPKK is involved in the vulval induction of C. elegans.",
author = "Makoto Koga and Yasumi Ohshima",
year = "1995",
month = "1",
day = "1",
doi = "10.1016/0925-4773(95)00417-3",
language = "English",
volume = "53",
pages = "15--22",
journal = "Mechanisms of Development",
issn = "0925-4773",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans

AU - Koga, Makoto

AU - Ohshima, Yasumi

PY - 1995/1/1

Y1 - 1995/1/1

N2 - The vulva of the nematode Caenorhabditis elegans develops from the three vulval precursor cells (VPCs) that are induced by a signal from the gonadal anchor cell. This signal is thought to be mediated by a receptor tyrosine kinase (RTK) in the VPCs to a downstream signal transduction pathway. A mitogen-activated protein kinase kinase (MAPKK) has been found to be one of the major components of an RTK pathway in other organisms. We expressed a wild type and an activated cDNA of Dsorl, a Drosophila MAPKK, in each of the three vulvaless mutants lin-3, let-23 and lin-45. The expression of an activated form of Dsorl in each of the mutants effectively induced a normal, functional vulva, that is, suppressed the vulvaless phenotype. The wild type Dsorl also suppressed albeit less effectively. These results suggest that a MAPKK is involved in the vulval induction of C. elegans.

AB - The vulva of the nematode Caenorhabditis elegans develops from the three vulval precursor cells (VPCs) that are induced by a signal from the gonadal anchor cell. This signal is thought to be mediated by a receptor tyrosine kinase (RTK) in the VPCs to a downstream signal transduction pathway. A mitogen-activated protein kinase kinase (MAPKK) has been found to be one of the major components of an RTK pathway in other organisms. We expressed a wild type and an activated cDNA of Dsorl, a Drosophila MAPKK, in each of the three vulvaless mutants lin-3, let-23 and lin-45. The expression of an activated form of Dsorl in each of the mutants effectively induced a normal, functional vulva, that is, suppressed the vulvaless phenotype. The wild type Dsorl also suppressed albeit less effectively. These results suggest that a MAPKK is involved in the vulval induction of C. elegans.

UR - http://www.scopus.com/inward/record.url?scp=0029166292&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029166292&partnerID=8YFLogxK

U2 - 10.1016/0925-4773(95)00417-3

DO - 10.1016/0925-4773(95)00417-3

M3 - Article

C2 - 8555107

AN - SCOPUS:0029166292

VL - 53

SP - 15

EP - 22

JO - Mechanisms of Development

JF - Mechanisms of Development

SN - 0925-4773

IS - 1

ER -