Sex chromosomes induce potentially deleterious gene expression imbalances that are frequently corrected by dosage compensation (DC). Three distinct molecular strategies to achieve DC have been previously described in nematodes, fruit flies, and mammals. Is this a consequence of distinct genomes, functional or ecological constraints, or random initial commitment to an evolutionary trajectory? Here, we study DC in the malaria mosquito Anopheles gambiae The Anopheles and Drosophila X chromosomes evolved independently but share a high degree of homology. We find that Anopheles achieves DC by a mechanism distinct from the Drosophila MSL complex-histone H4 lysine 16 acetylation pathway. CRISPR knockout of Anopheles msl-2 leads to embryonic lethality in both sexes. Transcriptome analyses indicate that this phenotype is not a consequence of defective X chromosome DC. By immunofluorescence and ChIP, H4K16ac does not preferentially enrich on the male X. Instead, the mosquito MSL pathway regulates conserved developmental genes. We conclude that a novel mechanism confers X chromosome up-regulation in Anopheles Our findings highlight the pluralism of gene-dosage buffering mechanisms even under similar genomic and functional constraints.

中文翻译：

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不同的机制介导按蚊和果蝇的 X 染色体剂量补偿。

性染色体诱导潜在有害的基因表达失衡，通常通过剂量补偿 (DC) 来纠正。以前在线虫、果蝇和哺乳动物中已经描述了三种不同的分子策略来实现 DC。这是不同基因组、功能或生态限制或对进化轨迹的随机初始承诺的结果吗？在这里，我们研究了疟疾蚊子冈比亚按蚊中的DC 。按蚊和果蝇X 染色体独立进化，但具有高度的同源性。我们发现按蚊通过与果蝇MSL 复合物-组蛋白 H4 赖氨酸 16 乙酰化途径不同的机制实现 DC 。CRISPR敲除按蚊 msl-2导致两性胚胎致死。转录组分析表明这种表型不是 X 染色体 DC 缺陷的结果。通过免疫荧光和 ChIP，H4K16ac 不会优先富集雄性 X。相反，蚊子 MSL 途径调节保守的发育基因。我们得出结论，一种新的机制使按蚊中的X 染色体上调我们的研究结果强调了基因剂量缓冲机制的多样性，即使在相似的基因组和功能限制下也是如此。