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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Biochim Biophys Acta. 2012 Jun 15;1830(2):2375–2384. doi: 10.1016/j.bbagen.2012.06.005

Figure 2. Antagonism between Dpp and JAK/STAT signaling regulates GATA:FOG complex formation to control cell fate choice.

Figure 2

(A) The GATA factor and JAK/STAT signaling co-activate dFOG gene expression. dFOG binds to SrpNC to form the GATA:FOG complex, which promotes stem-like cell multipotency and blocks differentiation. Dpp represses GATA expression and downregulates dFOG expression and complex formation. This limits the size of the stem-like cell pool. JAK/STAT signaling is initially downregulated during immune challenge (not shown). This promotes stem-like cell progression to the committed precursor stage by limiting GATA:FOG formation. (B) Later, JAK/STAT signaling is required for lamellocyte differentiation in response to immune challenge. However, JAK/STAT signaling continues to promote formation of the GATA:FOG complex. In order to counter this repressive effect, Dpp limits formation of the GATA:FOG complex to promote lamellocyte differentiation. Multipotent medullary zone (MZ) stem-like cells are depicted in blue. Differentiating cells of the cortical zone (CZ) are depicted in tan. Red arrows and blocked lines indicate pathways that maintain multipotency and block differentiation; green arrows and blocked lines indicate pathways that promote differentiation. dFOG is depicted in italics to indicate that gene expression is upregulated by the GATA factor Srp and JAK/STAT signaling.