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The PHOA and PHOB Cyclin-Dependent Kinases Perform an Essential Function in Aspergillus nidulans.

Authors :
Xiaowei Dou, Nancy P.
Dongliang Wu, Nancy P.
Weiling An, Nancy P.
Davies, Jonathan
Hashmi, Shahr B.
Ukil, Leena
Osmani, Stephen A.
Source :
Genetics. Nov2003, Vol. 165 Issue 3, p1105-1115. 11p. 3 Color Photographs, 4 Black and White Photographs, 3 Diagrams, 1 Chart, 8 Graphs.
Publication Year :
2003

Abstract

Unlike Pho85 of Saccharomyces cerevisiae, the highly related PHOA cyclin-dependent kinase (CDK) of Aspergillus nidulans plays no role in regulation of enzymes involved in phosphorous acquisition but instead modulates differentiation in response to environmental conditions, including limited phosphorous. Like PHO85, Aspergillus phoA is a nonessential gene. However, we find that expression of dominant-negative PHOA inhibits growth, suggesting it may have an essential but redundant function. Supporting this we have identified another cyclin-dependent kinase, PHOB, which is 77% identical to PHOA. Deletion of phoB causes no phenotype, even under phosphorous-limited growth conditions. To investigate the function of phoA/phoB, double mutants were selected from a cross of strains containing null alleles and by generating a temperature-sensitive allele of phoA in a ΔphoB background. Double-deleted ascospores were able to germinate but had a limited capacity for nuclear division, suggesting a cell cycle defect. Longer germination revealed morphological defects. The temperature-sensitive phoA allele caused both nuclear division and polarity defects at restrictive temperature, which could be complemented by expression of mammalian CDK5. Therefore, an essential function exists in A. nidulans for the Pho85-1ike kinase pair PHOA and PHOB, which may involve cell cycle control and morphogenesis. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00166731
Volume :
165
Issue :
3
Database :
Academic Search Index
Journal :
Genetics
Publication Type :
Academic Journal
Accession number :
12076009
Full Text :
https://doi.org/10.1093/genetics/165.3.1105