fhl1 gene of the fission yeast regulates transcription of meiotic genes and nitrogen starvation response, downstream of the TORC1 pathway

Emese Pataki, Ronit Weisman, Matthias Sipiczki, Ida Miklos

פרסום מחקרי: פרסום בכתב עתמאמרביקורת עמיתים

תקציר

Environmental changes, such as nutrient limitation or starvation induce different signal transducing pathways, which require coordinated cooperation of several genes. Our previous data revealed that the fhl1 fork-head type transcription factor of the fission yeast could be involved in sporulation, which was typically induced under poor conditions. Since the exact role of Fhl1 in this process was not known, we wanted to identify its downstream targets and to investigate its possible cooperation with another known regulator of sporulation. Gene expression and Northern blot analysis of the fhl1∆ mutant strain revealed the target genes involved in mating and sporulation. Our results also showed that Fhl1 could regulate nutrient sensing, the transporter and permease genes. Since the majority of these genes belonged to the nitrogen starvation response, the possible cooperation of fhl1 and tor2 was also investigated. Comparison of their microarray data and the expression of fhl1+ from a strong promoter in the tor2-ts mutant cells suggested that one part of the target genes are commonly regulated by Fhl1 and Tor2. Since the expression of fhl1+ from a strong promoter could rescue rapamycin and temperature sensitivity and suppressed the hyper-sporulation defect of the tor2-ts mutant cells, we believe that Fhl1 acts in TOR signaling, downstream of Tor2. Thus, this work shed light on certain novel details of the regulation of the sexual processes and a new member of the TOR pathway, but further experiments are needed to confirm the involvement of Fhl1 in nutrient sensing.

שפה מקוריתאנגלית
עמודים (מ-עד)91-101
מספר עמודים11
כתב עתCurrent Genetics
כרך63
מספר גיליון1
מזהי עצם דיגיטלי (DOIs)
סטטוס פרסוםפורסם - 1 פבר׳ 2017

הערה ביבליוגרפית

Publisher Copyright:
© 2016, Springer-Verlag Berlin Heidelberg.

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