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Development. 2017 Oct 15;144(20):3808-3818. doi: 10.1242/dev.146902. Epub 2017 Sep 11.

The TAF10-containing TFIID and SAGA transcriptional complexes are dispensable for early somitogenesis in the mouse embryo.

Bardot P1,2,3,4, Vincent SD5,2,3,4, Fournier M1,2,3,4, Hubaud A1,2,3,4, Joint M1,2,3,4, Tora L1,2,3,4, Pourquié O1,2,3,4.

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Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch 67400, France.
Centre National de la Recherche Scientifique, UMR7104, Illkirch 67400, France.
Institut National de la Santé et de la Recherche Médicale, U964, Illkirch 67400, France.
Université de Strasbourg, Illkirch 67400, France.
Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch 67400, France


During development, tightly regulated gene expression programs control cell fate and patterning. A key regulatory step in eukaryotic transcription is the assembly of the pre-initiation complex (PIC) at promoters. PIC assembly has mainly been studied in vitro, and little is known about its composition during development. In vitro data suggest that TFIID is the general transcription factor that nucleates PIC formation at promoters. Here we show that TAF10, a subunit of TFIID and of the transcriptional co-activator SAGA, is required for the assembly of these complexes in the mouse embryo. We performed Taf10 conditional deletions during mesoderm development and show that Taf10 loss in the presomitic mesoderm (PSM) does not prevent cyclic gene transcription or PSM segmental patterning, whereas lateral plate differentiation is profoundly altered. During this period, global mRNA levels are unchanged in the PSM, with only a minor subset of genes dysregulated. Together, our data strongly suggest that the TAF10-containing canonical TFIID and SAGA complexes are dispensable for early paraxial mesoderm development, arguing against the generic role in transcription proposed for these fully assembled holo-complexes.


Conditional knockout; Mouse; Paraxial mesoderm; Presomitic mesoderm; Proteomic; RNA polymerase II; TATA binding protein

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