mus-52 disruption and metabolic regulation in Neurospora crassa: Transcriptional responses to extracellular phosphate availability

Autor(es)

Martins, Maira P. ^[1] ; Gomes, Eriston V. ^[1] ; Sanches, Pablo R. ^[1] ; Pedersoli, Wellington R. ^[1] ; Martinez-Rossi, Nilce M. ^[1] ; Rossi, Antonio ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Genet, Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: PLoS One; v. 13, n. 4 APR 18 2018.
• Citações Web of Science: 1

Resumo

Advances in the understanding of molecular systems depend on specific tools like the disruption of genes to produce strains with the desired characteristics. The disruption of any mutagen sensitive (mus) genes in the model fungus Neurospora crassa, i.e. mus-51, mus-52, or mus-53, orthologous to the human genes KU70, KU80, and LIG4, respectively, provides efficient tools for gene targeting. Accordingly, we used RNA-sequencing and reverse transcription-quantitative polymerase chain reaction amplification techniques to evaluate the effects of mus-52 deletion in N. crassa gene transcriptional modulation, and thus, infer its influence regarding metabolic response to extracellular availability of inorganic phosphate (Pi). Notably, the absence of MUS-52 affected the transcription of a vast number of genes, highlighting the expression of those coding for transcription factors, kinases, circadian clocks, oxi-reduction balance, and membrane- and nucleolus-related proteins. These findings may provide insights toward the KU molecular mechanisms, which have been related to telomere maintenance, apoptosis, DNA replication, and gene transcription regulation, as well as associated human conditions including immune system disorders, cancer, and aging. (AU)

• Processo FAPESP: 16/04274-6 - Fatores de transcrição e sinalização celular
• Beneficiário: Eriston Vieira Gomes
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 14/03847-7 - Caracterização molecular de mecanismos envolvidos na patogenicidade e sinalização celular em fungos
• Beneficiário: Nilce Maria Martinez-Rossi
• Modalidade de apoio: Auxílio à Pesquisa - Temático