Development of Sexual Dimorphism Through the Adrenal Cortex, Caused by Androgen-Induced Global Gene Suppression

Takahashi, Fumiya; Baba, Takashi; Christianto, Antonius; Yanai, Shogo; Ishiwata, Keisuke; Nakabayashi, Kazuhiko; Hata, Kenichiro; Ishii, Takemochi; Hasegawa, Tomonobu; Choi, Man Ho; Morohashi, Ken-ichirou

doi:10.2139/ssrn.4425878

Cited by 1 publication

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“…31 It has been shown that the differential presence of androgens between sexes influences the magnitude of gene expression in other tissues. 32 The possible cooperative interaction between clock components, sex hormones, and their receptors could mediate the differential targeting and activation of circadian gene expression. However, sex hormone receptor motifs are not enriched by DEGs between sexes.…”

Section: Discussionmentioning

confidence: 99%

New role for cardiomyocyteBmal1in the regulation of sex-specific heart transcriptomes

Zhang,

Procopio,

Ding

et al. 2024

Preprint

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It has been well established that cardiovascular diseases exhibit significant differences between sexes in both preclinical models and humans. In addition, there is growing recognition that disrupted circadian rhythms can contribute to the onset and progression of cardiovascular diseases. However, little is known about sex differences between the cardiac circadian clock and circadian transcriptomes in mice. Here, we show that the the core clock genes are expressed in common in both sexes but the circadian transcriptome of the mouse heart is very sex-specific. Hearts from female mice expressed significantly more rhythmically expressed genes (REGs) than male hearts and the temporal pattern of REGs was distinctly different between sexes. We next used a cardiomyocyte-specific knock out of the core clock gene, Bmal1, to investigate its role in sex-specific gene expression in the heart. All sex differences in the circadian transcriptomes were significantly diminished with cardiomyocyte-specific loss of Bmal1. Surprisingly, loss of cardiomyocyte Bmal1 also resulted in a roughly 8-fold reduction in the number of all the differentially expressed genes between male and female hearts. We conclude that cardiomyocyte-specific Bmal1, and potentially the core clock mechanism, is vital in conferring sex-specific gene expression in the adult mouse heart.

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Section: Discussionmentioning

confidence: 99%