High impact information on NRG1

• We show that growth in serum at 37 degrees C, a potent inducer of filamentous growth, causes a reduction of NRG1 mRNA, suggesting that filamentous growth is induced by the down-regulation of NRG1 [1].
• These genes constitute a subset of those under Tup1 control, providing further evidence that Nrg1 acts by recruiting Tup1 to target genes [1].
• We show that Nrg1 and Rim101 bind simultaneously to adjacent target sites within the NRE in vitro and act as corepressors in vivo [2].
• NRG1 and SFL1 expression requires the Srb8-11 complex, and correspondingly, the Srb8-11 complex is also necessary for STA1 repression [3].
• Glucose repression of STA1 expression is mediated by the Nrg1 and Sfl1 repressors and the Srb8-11 complex [3].

Biological context of NRG1

• The NRG1 gene encodes a 25-kDa C2H2 zinc finger protein which specifically binds to two regions in the upstream activation sequence of the STA1 gene, as judged by gel retardation and DNase I footprinting analyses [4].
• In accord with these findings, mutation of NRG1 and NRG2 enhanced the resistance of cells to salt and oxidative stress and decreased tolerance to freezing [5].
• Deletion mutations of the Rim101p repression targets NRG1 and SMP1 suppress rim101Delta mutant defects in ion tolerance, haploid invasive growth, and sporulation [6].
• The transcription factor Rim101p governs ion tolerance and cell differentiation by direct repression of the regulatory genes NRG1 and SMP1 in Saccharomyces cerevisiae [6].
• Previously, we found that expression of the C-terminally truncated form of NRG1 (NRG1(1-470)) on a multicopy plasmid increases the hydrophobicity of the cell surface, conferring flor formation on the non-flor laboratory strain [7].

Associations of NRG1 with chemical compounds

• The expression of NRG1 itself is inhibited in the absence of glucose [4].
• Two-hybrid and glutathione S-transferase pull-down experiments show an interaction of Nrg1 with Ssn6 both in vivo and in vitro [4].
• Disruption of the Nrg1p-repressed gene FLO11, which encodes a cell surface glycoprotein that functions as a flocculin or an adhesin, abolished flor formation [8].

Other interactions of NRG1

• The Mig1-independent role depends on Nrg1p [9].
• Expression of NRG1 RNA is glucose repressed, whereas NRG2 RNA levels are nearly constant [10].
• Deletion of the NRG1 and NRG2 genes suppressed the defects of a snf1 mutant in all of these processes [11].
• A key target is the gene ENA1, encoding a Na(+)-ATPase, whose induction by alkaline pH has been shown to involve calcineurin and the Rim101/Nrg1 pathway [12].
• Disruption of the NRG1 gene causes a fivefold increase in the level of the STA1 transcript in the presence of glucose [4].

Analytical, diagnostic and therapeutic context of NRG1

• Chromatin immunoprecipitation assays showed that Nrg1 and Nrg2 bind DNA both in the presence and absence of glucose [10].
• In silico analysis of the 1.9-kb promoter sequence cloned by inverse PCR revealed the presence of several putative regulatory elements, most notably a 19-bp sequence containing six overlapping copies of the Saccharomyces cerevisiae Nrg1p binding sequence [13].

References