ArticleNature communications2022
Specificity of the Hox member Deformed is determined by transcription factor levels and binding site affinities.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Detection of Protein-Nucleic Acid Interaction by Electrophoretic Mobility Shift Assay.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Hox gene-specific cellular targeting using split intein Trojan exons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Enhancer-promoter interactions can form independently of genomic distance and be functional across TAD boundaries.Nucleic acids research · 2024Article
- Deep flanking sequence engineering for efficient promoter design using DeepSEED.Nature communications · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hox proteins have similar binding specificities in vitro, yet they control different morphologies in vivo. This paradox has been partially solved with the identification of Hox low-affinity binding sites. However, anterior Hox proteins are more promiscuous than posterior Hox proteins, raising the question how anterior Hox proteins achieve specificity. We use the AP2x enhancer, which is activated in the maxillary head segment by the Hox TF Deformed (Dfd). This enhancer lacks canonical Dfd-Exd sites but contains several predicted low-affinity sites. Unexpectedly, these sites are strongly bound by Dfd-Exd complexes and their conversion into optimal Dfd-Exd sites results only in a modest increase in binding strength. These small variations in affinity change the sensitivity of the enhancer to different Dfd levels, resulting in perturbed AP-2 expression and maxillary morphogenesis. Thus, Hox-regulated morphogenesis seems to result from the co-evolution of Hox binding affinity and Hox dosage for precise target gene regulation.
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Registered trials
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