Divergent non-coding transcription – University of Copenhagen

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Divergent non-coding transcription

Divergent non-coding transcription (DNC) describes non-coding transcription from gene promoters in the opposite direction with respect to the direction of gene transcription. DNC has been described in wide range of organisms (e.g. human, mouse, yeast) and is responsible for a large proportion of generated lncRNA in cells.

Despite the conservation of DNC, what purpose it serves is currently unclear. DNC likely affect gene expression in multiple ways, related to our interest in the functional consequences of non-coding transcription. DNC is selectively removed by RNA degradation as part of the mechanism terminating DNC transcription. This mechanism ensures DNC doesn’t accumulate, but how are cells determining how much DNC is made in the first place?

We recently identified a chromatin-based mechanism that controls DNC production from a quarter of yeast promoters and characterizing this mechanism further in budding yeast and Arabidopsis (1). We aim to use our knowledge of the mechanisms controlling DNC to design strategies that systematically query DNC functions.

(1) Marquardt S, Escalante-Chong R, Pho N, Wang J, Churchman S, Springer M, Buratowski S. A chromatin-based mechanism for limiting divergent non-coding transcriptionCell. 2014 Jun 19;157(7):1712-23.


Figure: Divergent non-coding transcription describes non-coding transcription from gene promoters in the opposite direction respective to gene transcription. DNC is selectively targeted by RNA degradation pathways that are linked to non-coding transcript termination (e.g. nuclear exosome). B.) We are identifying factors that determine how much DNC is generated in the first place by performing genetic screens in yeast.

Replacing the endogenous transcripts of the divergent PPT1/SUT129 promoter with fluorescent proteins helps us to quantify DNC in our screens. C.) We identified a chromatin mechanism that determines how much DNC is produced from yeast promoters*. An important component of this mechanism is the selective exchange of the -1 nucleosome that blocks DNC. We have identified chromatin remodeling and exchange factors that are linked to the acetylation of the conserved histone tail residue lysine-56 (K56ac).