Disease relevance of SPT16

• In contrast, showing a random nucleosome structure, YAT1 and Escherichia coli lacZ are only mildly influenced by Spt16 depletion [1].

High impact information on SPT16

• Yeast SPT16/CDC68 is an essential gene that has been implicated in transcription and cell-cycle regulation [2].
• The chromatin-specific transcription elongation factor FACT comprises human SPT16 and SSRP1 proteins [2].
• Spt16 functions as a component of the yeast CP (Cdc68/Pob3) and mammalian FACT (facilitates chromatin transcription) complexes, which are involved in transcription elongation and DNA replication [3].
• Sas3 mediates interaction of the NuA3 complex with Spt16 both in vivo and in vitro [3].
• SSF1 is a member of an essential gene family and functions in the response to mating pheromones [4].

Biological context of SPT16

• Yeast Spt16/Cdc68 and Pob3 form a heterodimer that acts in both DNA replication and transcription [5].
• We show that at the nonpermissive temperature, cdc68-1 mutants arrest as unbudded cells with a 1C DNA content, consistent with a possible role for Cdc68 in the prereplicative stage of the cell cycle [6].
• Overexpression of Cdc68 in a pol1 mutant strain dramatically decreased cell viability, consistent with the formation or modulation of an essential complex by these proteins in vivo [6].
• The something about silencing protein, Sas3, is the catalytic subunit of NuA3, a yTAF(II)30-containing HAT complex that interacts with the Spt16 subunit of the yeast CP (Cdc68/Pob3)-FACT complex [3].
• We suggest that Cdc68 functions both in the assembly of repressive complexes that form on many intact promoters in vivo and in the relief of this repression during gene activation [7].

Associations of SPT16 with chemical compounds

• Nhp6 interacts with Spt16/Pob3, the yeast equivalent of the FACT elongation complex, consistent with nhp6ab cells being extremely sensitive to 6-azauracil (6-AU) [8].

Physical interactions of SPT16

• Mutations in the TOA2 subunit of TFIIA that disrupt TBP-TFIIA complex formation in vitro are also synthetically lethal with spt16 [9].

Regulatory relationships of SPT16

• Mutations in Sir Antagonist 1 (SAN1) suppress defects in SIR4 and SPT16 in Saccharomyces cerevisiae [10].
• In some cases this spt16 toa2 lethality is suppressed by overexpression of TBP or the Nhp6 architectural transcription factor that is also a component of yFACT [9].

Other interactions of SPT16

• These results suggest that Spt16-Pob3 and Nhp6 cooperate to function as a novel nucleosome reorganizing factor [5].
• This result suggests that there may be both a chromatin structure and a UAS-specific component to Cdc68 function at SWI4 [7].
• The decreased abundance of cyclin transcripts in cdc68-1 mutant cells, coupled with the suppression of cdc68-1-mediated START arrest by the CLN2-1 hyperactive allele of CLN2, shows that the CDC68 gene affects START through cyclin gene expression [11].
• We investigated relationships between three classes of these factors: (1) transcription elongation factors Spt4-Spt5, TFIIS, and Spt16; (2) the C-terminal heptapeptide repeat domain (CTD) of RNA polymerase II; and (3) protein kinases that phosphorylate the CTD and a phosphatase that dephosphorylates it [12].
• Sug1 modulates yeast transcription activation by Cdc68 [13].

Analytical, diagnostic and therapeutic context of SPT16

• Our findings suggest that the San1 protein antagonizes the transcriptional activator function of the Cdc68 protein [14].

References