Creation of EcR isoform-specific mutations in Drosophila melanogaster via local P element transposition, imprecise P element excision, and male recombination

G. E. Carney, A. Robertson, Melissa B Davis, M. Bender

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Collections of single P transposable-element insertion strains that currently inactivate more than 25% of essential Drosophila genes have proven to be a valuable tool for genome research in Drosophila melanogaster. For genes unrepresented in these collections, strategies including local P element transposition and transposase-induced imprecise excision can be used to inactivate or delete the gene of interest. Here we report our use of local P element transposition followed by imprecise P element excision and transposase-induced male recombination to generate two deficiencies specific for the EcR-A isoform of the ecdysone receptor (EcR) gene, and four larger deficiencies likely to affect multiple EcR functions. We also report here the determination of sequences flanking six EcR-B deficiencies generated in a previous imprecise excision screen. EcR-A encodes one of a family of three related nuclear receptor proteins that, together with the heterodimer partner USP, mediate ecdysone signaling during Drosophila development. Our results delineate sequences required in vivo for EcR-A function, as well as identifying EcR-A intron 1 sequences that are not essential for EcR function.

Original languageEnglish (US)
Pages (from-to)282-290
Number of pages9
JournalMolecular Genetics and Genomics
Volume271
Issue number3
DOIs
StatePublished - Apr 1 2004

Fingerprint

Drosophila melanogaster
Genetic Recombination
Protein Isoforms
Mutation
Transposases
Drosophila
Genes
Ecdysone
DNA Transposable Elements
ecdysone receptor
Essential Genes
Cytoplasmic and Nuclear Receptors
Nuclear Proteins
Introns
Sequence Analysis
Genome
Research

Keywords

  • EcR
  • Imprecise excision
  • Local transposition
  • Male recombination
  • P element

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

Cite this

Creation of EcR isoform-specific mutations in Drosophila melanogaster via local P element transposition, imprecise P element excision, and male recombination. / Carney, G. E.; Robertson, A.; Davis, Melissa B; Bender, M.

In: Molecular Genetics and Genomics, Vol. 271, No. 3, 01.04.2004, p. 282-290.

Research output: Contribution to journalArticle

@article{3286731538f44b50afbb1d22a8871ab1,
title = "Creation of EcR isoform-specific mutations in Drosophila melanogaster via local P element transposition, imprecise P element excision, and male recombination",
abstract = "Collections of single P transposable-element insertion strains that currently inactivate more than 25{\%} of essential Drosophila genes have proven to be a valuable tool for genome research in Drosophila melanogaster. For genes unrepresented in these collections, strategies including local P element transposition and transposase-induced imprecise excision can be used to inactivate or delete the gene of interest. Here we report our use of local P element transposition followed by imprecise P element excision and transposase-induced male recombination to generate two deficiencies specific for the EcR-A isoform of the ecdysone receptor (EcR) gene, and four larger deficiencies likely to affect multiple EcR functions. We also report here the determination of sequences flanking six EcR-B deficiencies generated in a previous imprecise excision screen. EcR-A encodes one of a family of three related nuclear receptor proteins that, together with the heterodimer partner USP, mediate ecdysone signaling during Drosophila development. Our results delineate sequences required in vivo for EcR-A function, as well as identifying EcR-A intron 1 sequences that are not essential for EcR function.",
keywords = "EcR, Imprecise excision, Local transposition, Male recombination, P element",
author = "Carney, {G. E.} and A. Robertson and Davis, {Melissa B} and M. Bender",
year = "2004",
month = "4",
day = "1",
doi = "10.1007/s00438-004-0976-x",
language = "English (US)",
volume = "271",
pages = "282--290",
journal = "Molecular and General Genetics",
issn = "1617-4615",
publisher = "Springer Verlag",
number = "3",

}

TY - JOUR

T1 - Creation of EcR isoform-specific mutations in Drosophila melanogaster via local P element transposition, imprecise P element excision, and male recombination

AU - Carney, G. E.

AU - Robertson, A.

AU - Davis, Melissa B

AU - Bender, M.

PY - 2004/4/1

Y1 - 2004/4/1

N2 - Collections of single P transposable-element insertion strains that currently inactivate more than 25% of essential Drosophila genes have proven to be a valuable tool for genome research in Drosophila melanogaster. For genes unrepresented in these collections, strategies including local P element transposition and transposase-induced imprecise excision can be used to inactivate or delete the gene of interest. Here we report our use of local P element transposition followed by imprecise P element excision and transposase-induced male recombination to generate two deficiencies specific for the EcR-A isoform of the ecdysone receptor (EcR) gene, and four larger deficiencies likely to affect multiple EcR functions. We also report here the determination of sequences flanking six EcR-B deficiencies generated in a previous imprecise excision screen. EcR-A encodes one of a family of three related nuclear receptor proteins that, together with the heterodimer partner USP, mediate ecdysone signaling during Drosophila development. Our results delineate sequences required in vivo for EcR-A function, as well as identifying EcR-A intron 1 sequences that are not essential for EcR function.

AB - Collections of single P transposable-element insertion strains that currently inactivate more than 25% of essential Drosophila genes have proven to be a valuable tool for genome research in Drosophila melanogaster. For genes unrepresented in these collections, strategies including local P element transposition and transposase-induced imprecise excision can be used to inactivate or delete the gene of interest. Here we report our use of local P element transposition followed by imprecise P element excision and transposase-induced male recombination to generate two deficiencies specific for the EcR-A isoform of the ecdysone receptor (EcR) gene, and four larger deficiencies likely to affect multiple EcR functions. We also report here the determination of sequences flanking six EcR-B deficiencies generated in a previous imprecise excision screen. EcR-A encodes one of a family of three related nuclear receptor proteins that, together with the heterodimer partner USP, mediate ecdysone signaling during Drosophila development. Our results delineate sequences required in vivo for EcR-A function, as well as identifying EcR-A intron 1 sequences that are not essential for EcR function.

KW - EcR

KW - Imprecise excision

KW - Local transposition

KW - Male recombination

KW - P element

UR - http://www.scopus.com/inward/record.url?scp=2342622016&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2342622016&partnerID=8YFLogxK

U2 - 10.1007/s00438-004-0976-x

DO - 10.1007/s00438-004-0976-x

M3 - Article

C2 - 14747942

AN - SCOPUS:2342622016

VL - 271

SP - 282

EP - 290

JO - Molecular and General Genetics

JF - Molecular and General Genetics

SN - 1617-4615

IS - 3

ER -