Somatic 'soluble' adenylyl cyclase isoforms are unaffected in Sacy tm1Lex/Sacy tm1Lex 'knockout' mice. Academic Article uri icon

Overview

MeSH

  • Alleles
  • Animals
  • Base Sequence
  • Brain
  • Cyclic AMP
  • DNA Primers
  • Genetic Techniques
  • Kidney
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Phenotype
  • Protein Isoforms
  • RNA Interference

MeSH Major

  • Adenylyl Cyclases

abstract

  • Mammalian Soluble adenylyl cyclase (sAC, Adcy10, or Sacy) represents a source of the second messenger cAMP distinct from the widely studied, G protein-regulated transmembrane adenylyl cyclases. Genetic deletion of the second through fourth coding exons in Sacy(tm1Lex)/Sacy(tm1Lex) knockout mice results in a male sterile phenotype. The absence of any major somatic phenotype is inconsistent with the variety of somatic functions identified for sAC using pharmacological inhibitors and RNA interference. We now use immunological and molecular biological methods to demonstrate that somatic tissues express a previously unknown isoform of sAC, which utilizes a unique start site, and which 'escapes' the design of the Sacy(tm1Lex) knockout allele. These studies reveal increased complexity at the sAC locus, and they suggest that the known isoforms of sAC play a unique function in male germ cells.

publication date

  • September 22, 2008

has subject area

  • Adenylyl Cyclases
  • Alleles
  • Animals
  • Base Sequence
  • Brain
  • Cyclic AMP
  • DNA Primers
  • Genetic Techniques
  • Kidney
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Phenotype
  • Protein Isoforms
  • RNA Interference

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2532759

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0003251

PubMed ID

  • 18806876

Additional Document Info

start page

  • e3251

volume

  • 3

number

  • 9