Analysis of a novel calcium auxotrophy in Aspergillus nidulans

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• 作者：Helen Findon ; Ana-Maria Calcagno-Pizarelli ; José ; L. Martí ; nez ; Anja Spielvogel ; Ane Markina-I&#xf1 ; arrairaegui ; Tanya Indrakumar ; José ; Ramos ; Miguel A. Pe&#xf1 ; alva ; Eduardo A. Espeso ; H
• 关键词：Aspergillus ; Calcium transport ; Cation homeostasis ; Ion pump ; Vacuolation ; Transcriptional regulation
• 刊名：Fungal Genetics and Biology
• 出版年：2010
• 出版时间：July 2010
• 年：2010
• 卷：47
• 期：7
• 页码：647-655
• 全文大小：789 K

文摘

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 cerevisiae NHA1, encoding a plasma membrane Na⁺/H⁺ antiporter effluxing Na⁺ and K⁺, and a non-null mutation in trkB, homologous to S. cerevisiae TRK1, encoding a plasma membrane high affinity K⁺ transporter, also suppress the calcium auxotrophy.