Mitotically heritable, RNA polymerase II-independent H3K4 dimethylation stimulates INO1 transcriptional memory
Abstract
For some inducible genes, the rate and molecular mechanism of transcriptional activation depends on the prior experiences of the cell. This phenomenon, called epigenetic transcriptional memory, accelerates reactivation and requires both changes in chromatin structure and recruitment of poised RNA Polymerase II (RNAPII) to the promoter. Memory of inositol starvation in budding yeast involves a positive feedback loop between transcription factor-dependent interaction with the nuclear pore complex and histone H3 lysine 4 dimethylation (H3K4me2). While H3K4me2 is essential for recruitment of RNAPII and faster reactivation, RNAPII is not required for H3K4me2. Unlike RNAPII-dependent H3K4me2 associated with transcription, RNAPII-independent H3K4me2 requires Nup100, SET3C, the Leo1 subunit of the Paf1 complex and, upon degradation of an essential transcription factor, is inherited through multiple cell cycles. The writer of this mark (COMPASS) physically interacts with the potential reader (SET3C), suggesting a molecular mechanism for the spreading and re-incorporation of H3K4me2 following DNA replication.
Data availability
The scripts used to analyze the competition experiments are available at https://github.com/jasonbrickner/SeqComp.
Article and author information
Author details
Funding
National Institute of General Medical Sciences (R35 GM136419)
- Bethany Sump
- Donna G Brickner
- Agustina D'Urso
- Seo Hyun Kim
- Jason H Brickner
National Institute of General Medical Sciences (R01 GM118712)
- Bethany Sump
- Donna G Brickner
- Agustina D'Urso
- Seo Hyun Kim
- Jason H Brickner
National Institute of General Medical Sciences (T32 GM008061)
- Agustina D'Urso
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2022, Sump et al.
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