Limits...
Mutual interdependence of splicing and transcription elongation.

Brzyżek G, Świeżewski S - Transcription (2015)

Bottom Line: The more nuanced view is that the rate of transcription contributes to splicing regulation.On the other hand there is accumulating evidence that splicing has an active role in controlling transcription elongation by DNA-dependent RNA polymerase II (RNAP II).We briefly review those mechanisms and propose a unifying model where splicing controls transcription elongation to provide an optimal timing for successive rounds of splicing.

View Article: PubMed Central - PubMed

Affiliation: a Institute of Biochemistry and Biophysics; Polish Academy of Sciences ; Warsaw , Poland.

ABSTRACT
Transcription and splicing are intrinsically linked, as splicing needs a pre-mRNA substrate to commence. The more nuanced view is that the rate of transcription contributes to splicing regulation. On the other hand there is accumulating evidence that splicing has an active role in controlling transcription elongation by DNA-dependent RNA polymerase II (RNAP II). We briefly review those mechanisms and propose a unifying model where splicing controls transcription elongation to provide an optimal timing for successive rounds of splicing.

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Schematic representation of the transcription–splicing mutual dependency. Splicing controls transcription elongation of consecutive RNAP II molecules to provide an optimal timing for successive rounds of splicing. Blue arrow represents RNAP II transcription elongation rate effect on splice site selection by spliceosome. Green arrow represents spliceosome effect on transcription.
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f0001: Schematic representation of the transcription–splicing mutual dependency. Splicing controls transcription elongation of consecutive RNAP II molecules to provide an optimal timing for successive rounds of splicing. Blue arrow represents RNAP II transcription elongation rate effect on splice site selection by spliceosome. Green arrow represents spliceosome effect on transcription.

Mentions: Based on those data a kinetic coupling model has been proposed.4 This model predicts that when 2 alternative splice sites (SS) of similar strength compete, the slowdown of RNAP II elongation would favor the upstream SS while the faster elongation would favor the downstream SS. This model has gained strong support from studies using fast/slow RNAP II mutants,5 chemical modulators of RNAP II elongation rate6 and alternative splice site selection defects in elongation factors mutants7 (Fig. 1 upper panel). We have recently inhibited in Arabidopsis RNAP II elongation by 6AU treatment and interference of RNAP II endonucleolytic cleavage by mutations in Transcription Elongation Factor S-II (TFIISmut). As predicted by the kinetic coupling model we observed a preferential selection of upstream splices sites.8 In addition, the analysis of RNAP II occupancy in TFIISmut background revealed a localized increase of RNAP II levels at the alternative splice sites rather than a uniform effect on RNAP II occupancy.8Figure 1.


Mutual interdependence of splicing and transcription elongation.

Brzyżek G, Świeżewski S - Transcription (2015)

Schematic representation of the transcription–splicing mutual dependency. Splicing controls transcription elongation of consecutive RNAP II molecules to provide an optimal timing for successive rounds of splicing. Blue arrow represents RNAP II transcription elongation rate effect on splice site selection by spliceosome. Green arrow represents spliceosome effect on transcription.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581361&req=5

f0001: Schematic representation of the transcription–splicing mutual dependency. Splicing controls transcription elongation of consecutive RNAP II molecules to provide an optimal timing for successive rounds of splicing. Blue arrow represents RNAP II transcription elongation rate effect on splice site selection by spliceosome. Green arrow represents spliceosome effect on transcription.
Mentions: Based on those data a kinetic coupling model has been proposed.4 This model predicts that when 2 alternative splice sites (SS) of similar strength compete, the slowdown of RNAP II elongation would favor the upstream SS while the faster elongation would favor the downstream SS. This model has gained strong support from studies using fast/slow RNAP II mutants,5 chemical modulators of RNAP II elongation rate6 and alternative splice site selection defects in elongation factors mutants7 (Fig. 1 upper panel). We have recently inhibited in Arabidopsis RNAP II elongation by 6AU treatment and interference of RNAP II endonucleolytic cleavage by mutations in Transcription Elongation Factor S-II (TFIISmut). As predicted by the kinetic coupling model we observed a preferential selection of upstream splices sites.8 In addition, the analysis of RNAP II occupancy in TFIISmut background revealed a localized increase of RNAP II levels at the alternative splice sites rather than a uniform effect on RNAP II occupancy.8Figure 1.

Bottom Line: The more nuanced view is that the rate of transcription contributes to splicing regulation.On the other hand there is accumulating evidence that splicing has an active role in controlling transcription elongation by DNA-dependent RNA polymerase II (RNAP II).We briefly review those mechanisms and propose a unifying model where splicing controls transcription elongation to provide an optimal timing for successive rounds of splicing.

View Article: PubMed Central - PubMed

Affiliation: a Institute of Biochemistry and Biophysics; Polish Academy of Sciences ; Warsaw , Poland.

ABSTRACT
Transcription and splicing are intrinsically linked, as splicing needs a pre-mRNA substrate to commence. The more nuanced view is that the rate of transcription contributes to splicing regulation. On the other hand there is accumulating evidence that splicing has an active role in controlling transcription elongation by DNA-dependent RNA polymerase II (RNAP II). We briefly review those mechanisms and propose a unifying model where splicing controls transcription elongation to provide an optimal timing for successive rounds of splicing.

Show MeSH