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Sabath, K.

Publications and source records attributed to Sabath, K..

2 recordsLinked to original sources

Activator-promoter compatibility in mammals: a CpG-Island-specific co-activator directly bridges transcription factors to TFIID

Transcription from CpG island (CGI) promoters controls the expression of two-thirds of mammalian genes, yet despite their prevalence, it remains unknown whether CGI-specific co-activators with intrinsic specificity (i.e. compatibility) for these promoters exist or by what mechanisms they might function. Here, we perform proteome-wide functional screens to identify more than fifty transcriptional activators that are intrinsically specific to CGI promoters, establishing that promoter-class-specific activators are a widespread feature of mammalian gene regulation. Among these, we identify Host Cell Factor 1 (Hcfc1) as the founding member of CGI-specific co-activators. Hcfc1 is essential for the expression of thousands of CGI-promoter-driven genes and acquires CGI-specificity through a two-step mechanism: CGI-associated transcription factors recruit Hcfc1 through its Kelch domain, and Hcfc1 in turn directly engages the general transcription factor TFIID through a dedicated activation domain. The Hcfc1-TFIID interaction overcomes a key rate-limiting step for CGI promoter initiation, TFIID recruitment, thereby directly enabling transcription. Hcfc1 thus functions as a promoter-class-specific bridge between CGI-bound transcription factors and the general transcription machinery, analogous to Mediator but with intrinsic promoter specificity. Together, we uncover a dedicated activation pathway for CGI promoters, reveal a fundamental mechanistic difference in transcription activation between promoter classes in mammals, and establish co-activator-promoter compatibility as a core principle in mammalian gene regulation.

molecular biology↗

Mechanistic basis of gene-specific transcription regulation by the Integrator complex

The Integrator complex (INT) regulates gene expression via premature transcription termination of RNA polymerase II (RNAP2) at promoter-proximal pausing sites. This attenuation of transcription is required for cellular response to external stimuli, cell differentiation and neurodevelopment. How gene-specific regulation is achieved by INT in an inducible manner remains unclear. Here, we identify two sites on INT subunits 13/14 that serve as direct binding hubs for diverse sets of sequence-specific transcription factors (TFs) and other transcription effector complexes. The TFs co-localize with INT genome-wide, increase INT abundance on target genes and co-regulate inducible transcriptional programs. Consistently, disruption of INT-TF contacts impairs sensory cilia formation in response to glucose starvation. Structural analysis places INTs TF binding hubs upstream of the transcription bubble when attached to paused RNAP2, consistent with simultaneous TF-promoter association. Our data establish TF-mediated recruitment of INT to promoters as a widespread mechanism for targeted and inducible transcription attenuation.

molecular biology↗