High impact information on SRB2

• In vitro transcription and template commitment assays confirm that SRB2 and SRB5 are components of a functional preinitiation complex and are required for efficient transcription initiation [1].
• SRB2 was previously isolated and shown to encode a 23 kd TBP-binding protein [1].
• Indeed, cells lacking SRB2 and cells lacking a large portion of the CTD exhibit the same set of conditional growth phenotypes and exhibit very similar defects in gene expression in vivo [2].
• Mutations of the pol II C-terminal domain (CTD), the CTD kinase Kin28 and the holoenzyme subunit Srb2 all inhibited the formation of 3' polymerases in response to activator [3].
• Mutations in the yeast SRB2 general transcription factor suppress hpr1-induced recombination and show defects in DNA repair [4].

Biological context of SRB2

• We have obtained genetic and molecular evidence that the hrs2-1 mutation, isolated as a suppressor of the hyperrecombination phenotype of hpr1 delta, is in the SRB2 gene, which encodes a component of the RNA polII holoenzyme [4].
• This indicates that mutations in the basal transcription factor SRB2 impair DNA repair of MMS-induced damage, which adds a new connection between transcription and DNA repair [4].
• A newly constructed srb2 delta allele restores the wild-type levels of deletions in hpr1 delta cells, indicating that the lack of a functional SRB2 transcription factor suppresses recombination between direct repeats [4].

Associations of SRB2 with chemical compounds

• The srb2 delta 10 mutants are temperature-sensitive, cold-sensitive and are inositol auxotrophs [5].
• On the other hand, the hrs2-1 mutation (renamed srb2-101), in which Gly150 has been changed to Asp, makes cells sensitive to long MMS treatments, a phenotype observed for the srb2 delta null allele only in a hpr1 delta background [4].

References