Immune-microenvironment interactions in health and disease

@article{AI2023,

title = {The sex-specific factor SOA controls dosage compensation in Anopheles mosquitoes},

author = {Kalita AI and Marois E and Kozielska M and Weissing FJ and Jaouen E and Möckel MM and, Rühle F and Butter F and Basilicata MF and Keller Valsecchi CI},

url = {https://www.nature.com/articles/s41586-023-06641-0},

doi = {10.1038/s41586-023-06641-0.},

year  = {2023},

date = {2023-09-28},

journal = {Nature},

volume = {623},

pages = {175–182},

abstract = {The Anopheles mosquito is one of thousands of species in which sex differences play a central part in their biology, as only females need a blood meal to produce eggs. Sex differentiation is regulated by sex chromosomes, but their presence creates a dosage imbalance between males (XY) and females (XX). Dosage compensation (DC) can re-equilibrate the expression of sex chromosomal genes. However, because DC mechanisms have only been fully characterized in a few model organisms, key questions about its evolutionary diversity and functional necessity remain unresolved1. Here we report the discovery of a previously uncharacterized gene (sex chromosome activation (SOA)) as a master regulator of DC in the malaria mosquito Anopheles gambiae. Sex-specific alternative splicing prevents functional SOA protein expression in females. The male isoform encodes a DNA-binding protein that binds the promoters of active X chromosomal genes. Expressing male SOA is sufficient to induce DC in female cells. Male mosquitoes lacking SOA or female mosquitoes ectopically expressing the male isoform exhibit X chromosome misregulation, which is compatible with viability but causes developmental delay. Thus, our molecular analyses of a DC master regulator in a non-model organism elucidates the evolutionary steps that lead to the establishment of a chromosome-specific fine-tuning mechanism.},

keywords = {Anopheles, M3i, marois, SOA},

pubstate = {published},

tppubtype = {article}

}