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. Author manuscript; available in PMC: 2020 Jan 15.
Published in final edited form as: Gen Comp Endocrinol. 2018 Nov 22;271:91–96. doi: 10.1016/j.ygcen.2018.11.012

Fig. 3. A positive feedback mechanism to enhance T3 activation of gene transcription through histone methylation.

Fig. 3.

T3 induces the expression of Dot1L directly at the transcription level (Matsuura et al. 2012a) and PRMT1 indirectly via transcriptional activation of cMyc by TR in the developing stem cells (Fujimoto et al. 2012; Okada et al. 2017). Dot1L and PRMT1 in turn function as TR coactivators to increase local histone methylations to enhance transcription (Fujimoto et al. 2012; Wen et al. 2017a). It is worth pointing out that there has been no direct evidence for the recruitment of Dot1L to TREs, although PRMT1 has been shown to be recruited by TR to TREs in the presence of T3 during metamorphosis (Matsuda et al. 2009).