Kss1 is the MAP kinase that primarily functions under conditions of nutrient deprivation such as the lack of nitrogen or glucose in the growth media. Under such conditions,Niraparib activated Kss1 executes a program that leads to the production of cell adhesion molecules, which promote the adherence of yeast cells and thus effectively transform the organism from vegetative to filamentous growth. This pathway is named the invasive or pseudohyphal growth pathway in haploid cells and filamentous pathway in diploid cells. In addition, Kss1 becomes activated in response to pheromone stimulation, but in this case the activation is very transient and is rapidly inactivated by Fus3 via unknown mechanism. Transcription factors that are under the control of Kss1 are Ste12 and Tec1. Ste12 is unique because it is essential for both the pheromone signaling pathway and the invasive growth pathway. In the pheromone pathway, activation of Fus3 promotes the formation of Ste12-Ste12 homodimer,AMN107 which binds to promoter regions that contain a DNA sequence named pheromone-response-element and drives gene expression specifically required for mating. In the invasive growth pathway, activation of Kss1 promotes the formation of a Ste12-Tec1 heterodimer, which binds to filamentation-response-element and promotes the expression of genes required for invasive growth, such as FLO11, whose gene product is an adhesion molecule. Several studies have been carried out to elucidate the mechanisms that regulate the activity of Ste12 and Tec1. It has been shown that two transcriptional repressors, i.e., Dig1/Rst1 and Dig2/Rst2, play important roles in repressing the transcrip-tion activity of Ste12 and Tec1. Some early reports suggest that phosphorylation of these two repressors by activated MAP kinases such as Kss1 somehow leads to de-repression of Ste12 and Tec1, although mutating all six candidate MAP kinase phosphor-ylation sites on Dig1 did not appear to significantly alter the transcriptional activity of Tec1.