High impact information on TEC1

• Notably, mutation of the phosphoacceptor site in Tec1, deletion of FUS3, or deletion of DIA2 results in a loss of signaling specificity such that pheromone pathway signaling erroneously activates filamentation pathway gene expression and invasive growth [1].
• Developmental specificity was found to require a transcription factor of the TEA/ATTS family, Tec1, which cooperates with Ste12 during filamentous and invasive growth [2].
• In vitro gel mobility shift experiments show that Cph2 directly binds to the two sterol regulatory element 1-like elements upstream of TEC1 [3].
• Interestingly, upstream sequences of all known hypha-specific genes are found to contain potential binding sites for Tec1, a regulator of hyphal development [3].
• When haploid invasive growth is stimulated by high-copy expression of TEC1, by expression of the dominant hypermorphic allele STE11-4 or by deletion of HOG1, Ty1 transposition is concomitantly activated [4].

Biological context of TEC1

• The sole element in the TEC1 promoter that has thus far been shown to control Tec1 function is the filament response element [5].
• This finding suggests a possible role for a homologue of Saccharomyces cerevisiae TEC1 during the activation of proteinase gene expression in C. albicans [6].
• Involvement of SRE element of Ty1 transposon in TEC1-dependent transcriptional activation [7].
• This report defines the sequences in Ty1 required for TEC1-dependent activation using a TDH3::lacZ reporter gene in which the UAS was replaced by different portions of a Ty1 or Ty2 element [7].
• Tec1p and Ste12p have been postulated to regulate these developmental processes primarily by cooperative binding to filamentous and invasion-responsive elements (FREs), which are combined enhancer elements that consist of a Tec1p-binding site (TCS) and an Stel2p-binding site (PRE) [8].

Associations of TEC1 with chemical compounds

• Swe1 is also required for pseudohyphal growth in the absence of Tec1 and for the induction of filamentation by butanol, a related phenomenon [9].
• Degradation requires Fus3 kinase activity and a MAPK phosphorylation site in Tec1 at threonine 273 [1].

Enzymatic interactions of TEC1

• We present evidence that, during mating, Fus3 phosphorylates Tec1 to downregulate this invasive growth-specific transcription factor and its target genes [10].

Regulatory relationships of TEC1

• In contrast, the Ste12p-dependent FRE control mechanism is sufficiently executed by the N-terminal portion of Tec1p, which contains the TEA/ATTS DNA-binding domain [8].
• CaTEC1 complements the pseudohyphal and invasive growth defect of haploid and diploid S. cerevisiae tec1/tec1 mutant cells and strongly activates the promoter of FLO11, a gene required for pseudohyphal growth [6].
• We suggest that Fus3-triggered Tec1 degradation is an important part of the transcriptional induction of mating genes during the pheromone response [11].

Other interactions of TEC1

• Activation of FLO11 may thus be the primary means by which Ste12p and Tec1p cause invasive growth [12].
• Signaling pathway-responsive transcription factors such as Ste12, Tec1, and Flo8 are known to mediate filamentation-specific transcription [13].
• Mutational analysis of TEC1 revealed that TCS control, FLO11 expression, and haploid invasive growth require the C terminus of Tec1p [8].
• Cross-talk in ste5-E756G cells was due to both increased activation of Kss1 and reduced Fus3-dependent degradation of the filamentation pathway transcription factor Tec1 [14].
• In addition, the transcriptional regulators encoded by YCR020C, YBR083W, and YPR199C were expressed differently in the two strains [15].

References