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. 2016 May 23;126(7):2452–2464. doi: 10.1172/JCI82956

Figure 9. Proposed model for SF-1 and TLX1 function during spleen development.

Figure 9

RA signaling starts at E13.5 and is confined in the outer mesothelial layer of the developing spleen, a domain negative for TLX1. On the contrary, SF-1 and TLX1 restrict RA signaling by promoting Cyp26b1 expression and RA degradation, and repression of RA nuclear receptors in the inner mesenchyme. In the absence of Sf-1 or Tlx1 the expression of Cyp26b1 is markedly reduced, thus causing increased RA content and activity. As a result, RA binds to nuclear receptors that activate RA-induced transcriptional programs. Under these conditions, RA signals in an autocrine (dashed arrows) and paracrine (solid arrows) fashion within the SPM, thus causing growth arrest due to premature cellular differentiation and reduced vasculogenesis. Thus, expression of SF-1 and TLX1 in the SPM is required to control RA signaling and ensure spleen development.