Transcriptome analysis of the Aspergillus nidulans AtmA (ATM, Ataxia-Telangiectasia mutated) null mutant.
ATM is a phosphatidyl-3-kinase-related protein kinase that functions as a central regulator of DNA damage response in eukaryotes. In humans, mutations in ATM cause the devastating neurodegenerative disease Ataxia-Telangiectasia. Previously, we characterized the homologue of ATM (AtmA) in the filamentous fungus Aspergillus nidulans. In addition to its expected role in the DNA damage response, we found that AtmA is also required for polarized hyphal growth. Our results suggested that AtmA probably regulates the function and/or localization of landmark proteins required for the formation of a polarity axis. Here, we extended these studies by investigating which pathways are influenced by AtmA during proliferation and polar growth by comparatively determining the transcriptional profile of A. nidulans wild-type and DeltaatmA mutant strains in different growth conditions. Our results indicate an important role of the pentose phosphate pathway in the fungal proliferation during endogenous DNA damage and polar growth monitored by the AtmA kinase. Furthermore, we identified several genes that have decreased mRNA expression in the DeltaatmA mutant that are involved in the formation of a polarized hyphae and control of polar growth; in the synthesis of phosphatidic acid (e.g. phospholipase D); in the ergosterol biosynthesis (plasma membrane microdomains, lipid rafts); and in intracellular trafficking.
Malavazi
Iran
I
Departamento de Ciências Farmacêuticas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, São Paulo, Brazil.
Savoldi
Marcela
M
da Silva Ferreira
Márcia Eliana
ME
Soriani
Frederico Marianetti
FM
Bonato
Pierina Sueli
PS
de Souza Goldman
Maria Helena
MH
Goldman
Gustavo H
GH
D001233:Aspergillus nidulans / Q000235:genetics* / Q000378:metabolism; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D004875:Ergosterol / Q000096:biosynthesis; D005656:Fungal Proteins / Q000235:genetics* / Q000378:metabolism; D017353:Gene Deletion; D020869:Gene Expression Profiling; D015966:Gene Expression Regulation, Fungal; D025301:Hyphae / Q000235:genetics / Q000254:growth & development; D053858:Metabolic Networks and Pathways; D020411:Oligonucleotide Array Sequence Analysis; D010427:Pentose Phosphate Pathway; D010712:Phosphatidic Acids / Q000096:biosynthesis; D011494:Protein Kinases / Q000235:genetics* / Q000502:physiology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics* / Q000378:metabolism; D021381:Protein Transport; D025521:Tumor Suppressor Proteins / Q000235:genetics* / Q000378:metabolism
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D005656:Fungal Proteins; D010712:Phosphatidic Acids; D025521:Tumor Suppressor Proteins; D011494:Protein Kinases; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases; D004875:Ergosterol