Signaling Specificity in Yeast

摘要

A central problem that continues to puzzle biologists is how cells translate myriad stimuli into highly specific responses. Signaling specificity is complicated in eukaryotic cells because signal transduction pathways that respond to different stimuliand perform distinct functions often share the same pathway components. In haploid budding yeast, for example, the mitogen-activated protein kinase (MAPK) cascades that regulate both mating and filamentous growth share the same three activating kinases—Ste20 MAPKKKK or PAK-type kinase, Stell MAPKKK, and Ste7 MAPKK (which are activated serially)—as well as the Ste 12 transcription factor (see the figure). Two separate MAPKs are activated by the same Ste7 MAPKK: Fus3, which is essential for the matingprogram, and Kssl, which is essential for the filamentous growth program (also called invasive growth in hap-loids and pseudohyphal development in diploids). Fus3 and Kssl are both activated in response to mating pheromone by the MAPK scaffold protein Ste5; Kssl also can be activated by cell surface proteins such as mucin (Msb2) and other conditions that promote invasive growth [(1—3)', see (4) for a summary of targets in the mating and invasive growth pathway]. How is pathway specificity maintained with so much redundancy? Two papers in a recent issue of Cell reveal how the Fus3 and Kss 1 MAPK signaling pathways are insulated from each other, ensuring smooth execution of the mating program without erroneous activation of the filamentous growth program (5, 6).