鱼类性别可塑性的分子机制

Research progress on molecular mechanisms of sex plasticity in fish

鱼类性别具有高度的可塑性,具体表现为天然性逆转、原发性逆转和次发性逆转。近年来,一系列研究都证明鱼类性别可塑性与雌激素密切相关。一旦阻断性腺雌激素的合成,无论是未分化还是已分化卵巢都将性逆转为精巢。鱼类的性别决定通路基因缺失诱导的性逆转也与雌激素相关。重要的是,发现生殖细胞的可塑性依赖于foxl3和dmrt1的同时存在,缺失其中一个都不能通过改变雌激素水平从而诱导性逆转。因此,foxl3和dmrt1是生殖细胞响应雌激素的关键基因。另外,表观遗传调控基因kdm6bb通过选择性剪接介导温度诱导的性逆转。这些研究增进了我们对鱼类性别可塑性分子机制的认识。

Fish have a high plasticity in sex due to existing germline stem cells,which are manifested as natural sex reversal,primary sex reversal and secondary sex reversal.In recent years,a series of studies have shown that the sex plasticity in fish is closely related to estrogen.Once the synthesis of gonadal estrogen is blocked,both undifferentiated and differentiated ovaries will reverse to the testes.Mutation of the male sex determining genes induced sex reversal in fish species,which can be rescued by disruption of estrogen synthesis.Importantly,sex plasticity of germ cells depends on the coexistence of foxl3 and dmrt1,and the absence of either cannot be rescued by altering estrogen levels.Therefore,foxl3 and dmrt1 are key genes in response to estrogen induction in germ cells.On the other hand,there has been great progress in the mechanism of fish sex plasticity regulated by epigenetics.For example,kdm6bb mediates temperature induced sex reversal through alternative splicing.These studies have promoted our understanding of the molecular mechanisms underlying sex plasticity in fish.