Transcription factors (TFs) exert their regulatory action by binding to DNA with specific sequence preferences. However, different TFs can partially share their binding sequences . This "redundancy" of binding defines a way URLanizing TFs in "motif families" that goes beyond the usual classification based on protein structural similarities. Since the TF binding preferences ultimately define the  target genes, the motif URLanization entails information about the structure of transcriptional regulation as it has been shaped by evolution. Focusing on the human lineage , we show that a one-parameter evolutionary model of the Birth-Death-Innovation type can explain the empirical repartition of TFs in motif families, thus identifying the relevant evolutionary forces at its origin . More importantly , the model allows to pinpoint few deviations in human from the neutral scenario it assumes: three over-expanded families corresponding to HOX and FOX type genes , a set of "singleton" TFs for which duplication seems to be selected against, and an higher-than-average rate of diversification of the binding preferences of TFs with a Zinc Finger DNA binding domain. Finally, a comparison of the TF motif URLanization in different eukaryotic species suggests an increase of redundancy of binding URLanism complexity.
Transcription factors (TFs) exert their regulatory action by binding to DNA with specific sequence preferences. However, different TFs can partially share their binding sequences due to their common evolutionary origin. This `redundancy' of binding defines a way URLanizing TFs in `motif families' by grouping TFs with similar binding preferences. Since these ultimately define the TF target genes, the motif URLanization entails information about the structure of transcriptional regulation as it has been shaped by evolution. Focusing on the human TF repertoire , we show that a one-parameter evolutionary model of the Birth-Death-Innovation type can explain the TF empirical ripartition in motif families, and allows to highlight the relevant evolutionary forces at the origin of URLanization. Moreover , the model allows to pinpoint few deviations from the neutral scenario it assumes: three over-expanded families (including HOX and FOX genes) , a set of `singleton' TFs for which duplication seems to be selected against, and a higher-than-average rate of diversification of the binding preferences of TFs with a Zinc Finger DNA binding domain. Finally, a comparison of the TF motif URLanization in different eukaryotic species suggests an increase of redundancy of binding URLanism complexity.
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. This "redundancy"
due to their common evolutionary origin. This `redundancy'
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"motif families" that goes beyond the usual classification based on protein structural similarities. Since the TF binding preferences
`motif families' by grouping TFs with similar binding preferences. Since these
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TF
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lineage
TF repertoire
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empirical repartition of TFs
TF empirical ripartition
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thus identifying
and allows to highlight
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its origin . More importantly
the origin of URLanization. Moreover
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in human
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corresponding to
(including
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type genes
genes)
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"singleton"
`singleton'
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an
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