Tissue-specific regulation of translational readthrough tunes functions of the 
traffic jam transcription factor

Karki, P.; Carney, T. D.; Maracci, C.; Yatsenko, A. S.; Shcherbata, H. R.; Rodnina, M. V.

doi:10.1093/nar/gkab1189

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Tissue-specific regulation of translational readthrough tunes functions of the traffic jam transcription factor

MPS-Authors

/persons/resource/persons206931

Karki, P.
Department of Physical Biochemistry, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons135076

Maracci, C.
Department of Physical Biochemistry, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons15723

Rodnina, M. V.
Department of Physical Biochemistry, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

3400868.pdf
(Publisher version), 5MB

Supplementary Material (public)

There is no public supplementary material available

Citation

Karki, P., Carney, T. D., Maracci, C., Yatsenko, A. S., Shcherbata, H. R., & Rodnina, M. V. (2022). Tissue-specific regulation of translational readthrough tunes functions of the traffic jam transcription factor. Nucleic Acids Research, 50(11), 6001-6019. doi:10.1093/nar/gkab1189.

Cite as: https://hdl.handle.net/21.11116/0000-000A-E928-3

Abstract

Translational readthrough (TR) occurs when the ribosome decodes a stop codon as a sense codon,
resulting in two protein isoforms synthesized from
the same mRNA. TR has been identified in several
eukaryotic organisms; however, its biological significance and mechanism remain unclear. Here, we
quantify TR of several candidate genes in
Drosophila
melanogaster and characterize the regulation of TR
in the large Maf transcription factor Traffic jam
(Tj). Using CRISPR/Cas9-generated mutant flies, we
show that the TR-generated Tj isoform is expressed
in a subset of neural cells of the central nervous
system and is excluded from the somatic cells of
gonads. Control of TR in Tj is critical for preservation of neuronal integrity and maintenance of reproductive health. The tissue-specific distribution of a
release factor splice variant, eRF1H, plays a critical
role in modulating differential TR of leaky stop codon
contexts. Finetuning of gene regulatory functions
of transcription factors by TR provides a potential
mechanism for cell-specific regulation of gene ex-pression.