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Figure 1 | BMC Systems Biology

Figure 1

From: Genetic and systems level analysis of Drosophila sticky/citron kinase and dFmr1 mutants reveals common regulation of genetic networks

Figure 1

sticky mutations rescue dFmr1 overexpression phenotypes in the Drosophila eye. (A) Scanning electron microscope visualization of eye developmental defects due to overexpression of dFmr1 by the sevenless promoter in a sticky wild-type background (sev:dFmr1, sti+/+). (B-C) One mutant copy of the sticky, sti3/+ or stiZ 3-5829/+dominantly suppresses the rough eye phenotype caused by sev:dFmr1 overexpression. (D-E) The crater-like necrotic adult eye tissue caused by the sev:dFmr1 overexpression (see arrows) is almost completely suppressed by one mutant copy of stiZ 3-5829/+. (F) Rho is known to directly activate sticky (solid arrow) and Rac is known to inhibit (solid bar) sticky activity. Other, unknown (?) developmental and cellular signals may also regulate sticky activity. We propose that both Ago1 and Fmrp activities are downstream of sticky, and that some wild-type or gain-of-function Ago1 and Fmrp dependant processes are sensitive to sticky. Dashed arrows indicate possible indirect interactions. This model is supported by the genetic interaction between sticky and dFmr1 shown above and that previously reported for sticky and Ago1 [8]. Both Ago1 and Fmrp are known to directly control microRNA mediated gene regulation (solid arrows). Fmrp also directly targets Rac1 mRNA for repression [28]. sticky and Fmrp proteins also control gene expression through heterochromatin gene silencing (bars and dashed arrows). It is not known whether these effects on heterochromatin are direct or indirect.

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