High impact information on HOT1

• A DNA sequence (HOT1) from the repeated ribosomal RNA gene cluster of Saccharomyces cerevisiae can stimulate genetic exchange when inserted at novel locations in the yeast genome [1].
• FOB1 was shown previously to be required for replication fork blocking (RFB) activity at RFB site in rDNA and for recombination hot-spot (HOT1) activity [2].
• In response to high osmolarity, Hot1 targets Hog1 to specific osmostress-responsive promoters [3].
• Unexpectedly, recruitment of RNA polymerase (Pol) II complex to target promoters does not depend on the phosphorylation of the Hot1 activator by the MAPK [3].
• In the ribosomal DNA of Saccharomyces cerevisiae, sequences in the nontranscribed spacer 3' of the 35S ribosomal RNA gene are important to the polar arrest of replication forks at a site called the replication fork barrier (RFB) and also to the cis-acting, mitotic hyperrecombination site called HOT1 [4].

Biological context of HOT1

• Osmotic stress-induced gene expression in Saccharomyces cerevisiae requires Msn1p and the novel nuclear factor Hot1p [5].
• FOB1 is required for recombination hot spot (HOT1) activity, which also requires the enhancer region, and for recombination within rDNA repeats [6].
• In Saccharomyces cerevisiae, HOT1-stimulated recombination has been implicated in maintaining homology between repeated ribosomal RNA genes [7].
• The trans-acting nuclear mutation hrm3-1 specifically reduces HOT1-dependent recombination and prevents cell growth at 37 degrees . The HRM3 gene is identical to DEG1 [7].
• Sch9p may affect signal transduction pathways which regulate proteins that are specifically required for HOT1-stimulated exchange [8].

Associations of HOT1 with chemical compounds

• The transcriptional response of Saccharomyces cerevisiae to osmotic shock. Hot1p and Msn2p/Msn4p are required for the induction of subsets of high osmolarity glycerol pathway-dependent genes [9].

Physical interactions of HOT1

• Studies on rad1 delta rad52-8 strains show that these mutations interact synergistically in the presence or absence of HOT1, resulting in low levels of recombination [10].

Regulatory relationships of HOT1

• In contrast, Hot1p has little influence on the osmotic stress induction of CTT1, where Msn1p appears to play a more prominent role [5].
• Compared to recombinants isolated from control strains that lack HOT1, HOT1-promoted His+ recombinants are more often homozygous for sequences distal to HIS4 [11].
• The Hot1 transcription factor acts downstream of the MAPK and regulates a subset of Hog1-responsive genes [3].

Other interactions of HOT1

• The rate of gene replacement but not excisive recombination is stimulated by HOT1 in rad1 delta rad52-8 strains [10].
• There is also a component of HOT1 activity that is independent of both RAD1 and RAD52 [10].
• Deletion of SCH9 decreases HOT1 and rDNA recombination but not other mitotic exchange [8].
• When HOT1 is inserted adjacent to both copies of HIS4, the frequency of His+ recombinants is increased approximately 10-fold [11].
• Ura- recombinants were increased only 2-fold when HOT1 and URA3 were on opposite homologues [12].

Analytical, diagnostic and therapeutic context of HOT1

• The recombination-stimulating sequence HOT1 is derived from the ribosomal DNA array of Saccharomyces cerevisiae and corresponds to sequences that promote transcription by RNA polymerase I. When inserted at a chromosomal location outside the ribosomal DNA array, HOT1 stimulates mitotic recombination in the adjacent sequences [13].

References