10.6084/m9.figshare.1468564.v6
Kevin Van Bortle
Kevin
Van Bortle
Aidan J Peterson
Aidan
J Peterson
Naomi Takenaka
Naomi
Takenaka
Michael B O'Connor
Michael
B O'Connor
Victor G Corces
Victor
G Corces
CTCF-dependent co-localization of canonical Smad signaling factors at architectural protein binding sites in <i>D. melanogaster</i>
Taylor & Francis Group
2015
BMP
chromatin
epigenetics
growth factor
Transcription
TGF-β signaling
2015-10-09 23:08:22
Journal contribution
https://tandf.figshare.com/articles/journal_contribution/CTCF_dependent_co_localization_of_canonical_Smad_signaling_factors_at_architectural_protein_binding_sites_in_i_D_melanogaster_i_/1468564
<p>The transforming growth factor β (TGF-β) and bone morphogenetic protein (BMP) pathways transduce extracellular signals into tissue-specific transcriptional responses. During this process, signaling effector Smad proteins translocate into the nucleus to direct changes in transcription, but how and where they localize to DNA remain important questions. We have mapped <i>Drosophila</i> TGF-β signaling factors Mad, dSmad2, Medea, and Schnurri genome-wide in Kc cells and find that numerous sites for these factors overlap with the architectural protein CTCF. Depletion of CTCF by RNAi results in the disappearance of a subset of Smad sites, suggesting Smad proteins localize to CTCF binding sites in a CTCF-dependent manner. Sensitive Smad binding sites are enriched at low occupancy CTCF peaks within topological domains, rather than at the physical domain boundaries where CTCF may function as an insulator. In response to Decapentaplegic, CTCF binding is not significantly altered, whereas Mad, Medea, and Schnurri are redirected from CTCF to non-CTCF binding sites. These results suggest that CTCF participates in the recruitment of Smad proteins to a subset of genomic sites and in the redistribution of these proteins in response to BMP signaling.</p>