Spt4-Spt5, a general transcription elongation factor for RNA polymerase II, also 
has roles in chromatin regulation. However, the relationships between these 
functions are not clear. Previously, we isolated suppressors of a Saccharomyces 
cerevisiae spt5 mutation in genes encoding members of the Paf1 complex, which 
regulates several cotranscriptional histone modifications, and Chd1, a chromatin 
remodeling enzyme. Here, we show that this suppression of spt5 can result from 
loss of histone H3 lysines 4 or 36 methylation, or reduced recruitment of Chd1 
or the Rpd3S complex. These spt5 suppressors also rescue the synthetic growth 
defects observed in spt5 mutants that also lack elongation factor TFIIS. Using a 
FLO8 reporter gene, we found that a chd1 mutation caused cryptic initiation of 
transcription. We further observed enhancement of cryptic initiation in chd1 
isw1 mutants and increased histone acetylation in a chd1 mutant. We suggest 
that, as previously proposed for H3 lysine 36 methylation and the Rpd3S complex, 
H3 lysine 4 methylation and Chd1 function to maintain normal chromatin 
structures over transcribed genes, and that one function of Spt4-Spt5 is to help 
RNA polymerase II overcome the repressive effects of these histone modifications 
and chromatin regulators on transcription.