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Eliminating SF-1 (NR5A1) sumoylation in vivo results in ectopic hedgehog signaling and disruption of endocrine development.

Developmental cell | 2011

Sumoylation is generally considered a repressive mark for many transcription factors. However, the in vivo importance of sumoylation for any given substrate remains unclear and is questionable because the extent of sumoylation appears exceedingly low for most substrates. Here, we permanently eliminated SF-1/NR5A1 sumoylation in mice (Sf-1(K119R, K194R, or 2KR)) and found that Sf-1(2KR/2KR) mice failed to phenocopy a simple gain of SF-1 function or show elevated levels of well-established SF-1 target genes. Instead, mutant mice exhibited marked endocrine abnormalities and changes in cell fate that reflected an inappropriate activation of hedgehog signaling and other potential SUMO-sensitive targets. Furthermore, unsumoylatable SF-1 mutants activated Shh and exhibited preferential recruitment to Shh genomic elements in cells. We conclude that the sumoylation cycle greatly expands the functional capacity of transcription factors such as SF-1 and is leveraged during development to achieve cell-type-specific gene expression in multicellular organisms.

Pubmed ID: 21820362 RIS Download

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Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: T32 DK007418
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK070024
  • Agency: NIDDK NIH HHS, United States
    Id: F32 DK079499-02
  • Agency: NIDDK NIH HHS, United States
    Id: T32 DK07418
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK070024-07
  • Agency: NIDDK NIH HHS, United States
    Id: F32 DK082100-03
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK070024-06
  • Agency: CIHR, Canada

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