The Grad Student Regulatory Network
In phd mutants, Ddl (Deadline) signaling causes UTDL (unrealistic to-do lists) to become phosphorylated and translocate to the nucleus to promote transcription of wka (workaholic). Acting in a feed-forward loop, wka activates the p10 (perfectionst) pathway. p10 enhances wka transcription by binding a conserved enhancer region ECR-INWO (I’m not worthy) upstream of wka. Above a certain threshold, wka also activates ins (insomia), dpr (depression), and dfl (dissatisfied family). Excess p10 is targeted for degradation by REL (real life) but in the presence of Dl (dumb luck) and DBL (double shot of espresso) may be able to activate dat (data) and apa (appeased advisor).
It has been shown that a point mutation in wka, which causes an amino acid change from Y to N at the p10 recognition site, interferes with the wka feed-forward mechanism. In other grad students a variant of dfl, which codes for a transcription factor, indirectly represses wka expression by turning on why (why am I doing this to myself). Both mutations rescue normal phenotypes.