Figure 2.

Putative molecular mechanism of the negative feedback action of estrogen on Kiss1 expression in the arcuate nucleus (ARC). Circulating estrogen seems to act on ARC kisspeptin neurons, in which estrogen-bound estrogen receptor α (ERα) coupled with an unknown transcriptional partner may repress Kiss1 expression via histone deacetylation and unwinding chromatin loops between the Kiss1 promoter and the 5′-intergenic regions of Kiss1 locus. In the absence of estrogen, ARC Kiss1 expression may be up-regulated by histone acetylation and chromatin loop formation between the Kiss1 promoter and the 5′-intergenic regions of the Kiss1 locus.