Fig. 6

A model summarizing the role of the HH signalling pathway and its primary transducer, GLI2, during mES cell cardiomyogenesis. a In this study, GLI2 expression was observed to positively regulate cardiac progenitor-enriched genes in mES cells (highlighted in green). The solid black arrows indicate HH/GLI2’s proposed direct regulation. The hollow green arrow marks the transition that is enhanced by GLI2. b GLI2-regulated enrichment of cardiac progenitor transcripts may be explained in part by the ability of the transcriptional activator form of GLI2 (GLI2A) (light green ellipses, B) - mediated via a functional HH signalling pathway (light blue ellipses) - to enrich BRG1 association at GLI2-specific Mef2c site C. This enrichment site is proximal to known SHF enhancer regions (I,II). Other cofactors (dash-outlined ellipses), including the remaining BAF complex members and other unidentified SHF-related transcription factors (?) may support this GLI2-mediated association. c When KAAD-cyclopamine inhibits HH signalling, GLI2 is likely degraded, which leads to a reduction of BRG1 association on Mef2c site C. Although we have not observed the formation of GLI2R in our system (data not shown), it is possible that GLI2 may be processed into GLI2R (orange truncated ellipses, C) when HH signalling is blocked [13]. Also, GLI3R (included in the orange truncated ellipses, C) may contribute to the repression of Mef2c expression. The downstream binding of either GLI2R or GLI3R to Mef2c has yet to be assessed ( )