Role of Trichoderma reesei mitogen-activated protein kinases (MAPKs) in cellulase formation

نویسندگان

  • Mingyu Wang
  • Meiling Zhang
  • Ling Li
  • Yanmei Dong
  • Yi Jiang
  • Kuimei Liu
  • Ruiqin Zhang
  • Baojie Jiang
  • Kangle Niu
  • Xu Fang
چکیده

BACKGROUND Despite being the most important cellulase producer, the cellulase-regulating carbon source signal transduction processes in Trichoderma reesei are largely unknown. Elucidating these processes is the key for unveiling how external carbon sources regulate cellulase formation, and ultimately for the improvement of cellulase production and biofuel production from lignocellulose. RESULTS In this work, the role of the mitogen-activated protein kinase (MAPK) signal transduction pathways on cellulase formation was investigated. The deletion of yeast FUS3-like tmk1 in T. reesei leads to improved growth and significantly improved cellulase formation. However, tmk1 deletion has no effect on the transcription of cellulase-coding genes. The involvement of the cell wall integrity maintenance governing yeast Slt2-like Tmk2 in cellulase formation was investigated by overexpressing tmk3 in T. reesei Δtmk2 to restore cell wall integrity. Transcriptional analysis found little changes in cellulase-coding genes between T. reesei parent, Δtmk2, and Δtmk2::OEtmk3 strains. Cell wall integrity decreased in T. reesei Δtmk2 over the parent strain and restored in Δtmk2::OEtmk3. Meanwhile, cellulase formation is increased in T. reesei Δtmk2 and then decreased in T. reesei Δtmk2::OEtmk3. CONCLUSIONS These investigations elucidate the role of Tmk1 and Tmk2 on cellulase formation: they repress cellulase formation, respectively, by repressing growth and maintaining cell wall integrity, while neither MAPK regulates the transcription of cellulase-coding genes. This work, together with the previous investigations, suggests that all MAPKs are involved in cellulase formation, while Tmk3 is the only MAPK involved in signal transduction for the regulation of cellulase expression on the transcriptional level.

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عنوان ژورنال:

دوره 10  شماره 

صفحات  -

تاریخ انتشار 2017