Transcriptome analysis of the Aspergillus nidulans AtmA (ATM, Ataxia-Telangiectasia mutated) null mutant
Article first published online: 14 SEP 2007
Volume 66, Issue 1, pages 74–99, October 2007
How to Cite
Malavazi, I., Savoldi, M., Da Silva Ferreira, M. E., Soriani, F. M., Bonato, P. S., De Souza Goldman, M. H. and Goldman, G. H. (2007), Transcriptome analysis of the Aspergillus nidulans AtmA (ATM, Ataxia-Telangiectasia mutated) null mutant. Molecular Microbiology, 66: 74–99. doi: 10.1111/j.1365-2958.2007.05885.x
- Issue published online: 14 SEP 2007
- Article first published online: 14 SEP 2007
- Accepted 23 July, 2007.
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 ΔatmA 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 ΔatmA 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.