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Abstract：
During in vitro fertilisation (IVF), pharmacological activation of the murine X chromosome-encoded receptor proteins Toll-like receptor (TLR) 7 and TLR8 reportedly results in male-biased litters by selectively disrupting the motility of X-bearing sperm cells. Thus-in the context of agonist treatment during IVF-these receptors act as \'suicidal\' segregation distorters that impair their own transmission to the next generation. Such behaviour would, from an evolutionary perspective, be strongly selected against if present during natural fertilisation. Consequently, TLR7/8 biology in vivo must differ significantly from this in vitro situation to allow these genes to persist in the genome. Here, we use our current understanding of male germ cell biology and TLR function as a starting point to explore the mechanistic and evolutionary aspects of this apparent paradox.
摘要：
在体外受精（IVF）期间，据报道,小鼠X染色体编码的受体蛋白Toll样受体(TLR)7和TLR8的药理激活通过选择性地破坏带有X的精子细胞的运动性而导致雄性偏向的窝。因此，在IVF期间的激动剂治疗的背景下，这些受体充当“自杀”隔离扭曲剂，损害其自身向下一代的传播。这种行为会,从进化的角度来看，如果在自然受精过程中存在，则强烈选择。因此,体内TLR7/8生物学必须与这种体外情况显着不同，以允许这些基因在基因组中持续存在。这里,我们以目前对男性生殖细胞生物学和TLR功能的理解为起点,探讨这一明显悖论的机制和进化方面.
