Article thumbnail

Analysis of a novel calcium auxotrophy in Aspergillus nidulans

By Helen Findon, Ana-Maria Calcagno-Pizarelli, José L. Martínez, Anja Spielvogel, Ane Markina-Iñarrairaegui, Tanya Indrakumar, José Ramos, Miguel A. Peñalva, Eduardo A. Espeso and Herbert N. Arst

Abstract

In Aspergillus nidulans a combination of null mutations in halA, encoding a protein kinase, and sltA, encoding a zinc-finger transcription factor having no yeast homologues, results in an elevated calcium requirement (‘calcium auxotrophy’) without impairing net calcium uptake. sltA− (±halA−) mutations result in hypertrophy of the vacuolar system. In halA−sltA− (and sltA−) strains, transcript levels for pmcA and pmcB, encoding vacuolar Ca2+-ATPase homologues, are highly elevated, suggesting a regulatory relationship between vacuolar membrane area and certain vacuolar membrane ATPase levels. Deletion of both pmcA and pmcB strongly suppresses the ‘calcium auxotrophy’. Therefore the ‘calcium auxotrophy’ possibly results from excessive vacuolar calcium sequestration, causing cytosolic calcium deprivation. Null mutations in nhaA, homologous to Saccharomyces cerevisiaeNHA1, encoding a plasma membrane Na+/H+ antiporter effluxing Na+ and K+, and a non-null mutation in trkB, homologous to S. cerevisiaeTRK1, encoding a plasma membrane high affinity K+ transporter, also suppress the calcium auxotrophy

Topics: Article
Publisher: Academic Press
OAI identifier: oai:pubmedcentral.nih.gov:2884188
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)

  • To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.

    Suggested articles