TFIIS promotes the intrinsic ability of RNA polymerase II to cleave the 3'-end 
of the newly synthesized RNA. This stimulatory activity of TFIIS, which is 
dependent upon Rpb9, facilitates the resumption of transcription elongation when 
the polymerase stalls or arrests. While TFIIS has a pronounced effect on 
transcription elongation in vitro, the deletion of DST1 has no major effect on 
cell viability. In this work we used a genetic approach to increase our 
knowledge of the role of TFIIS in vivo. We showed that: (1) dst1 and rpb9 
mutants have a synthetic growth defective phenotype when combined with fyv4, 
gim5, htz1, yal011w, ybr231c, soh1, vps71, and vps72 mutants that is exacerbated 
during germination or at high salt concentrations; (2) TFIIS and Rpb9 are 
essential when the cells are challenged with microtubule-destabilizing drugs; 
(3) among the SDO (synthetic with Dst one), SOH1 shows the strongest genetic 
interaction with DST1; (4) the presence of multiple copies of TAF14, SUA7, 
GAL11, RTS1, and TYS1 alleviate the growth phenotype of dst1 soh1 mutants; and 
(5) SRB5 and SIN4 genetically interact with DST1. We propose that TFIIS is 
required under stress conditions and that TFIIS is important for the transition 
between initiation and elongation in vivo.