The sex-specific factor SOA controls dosage compensation in Anopheles mosquitoes

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 f...

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Bibliographic Details
Published in:Nature (London) 2023-11, Vol.623 (7985), p.175-182
Main Authors: Kalita, Agata Izabela, Marois, Eric, Kozielska, Magdalena, Weissing, Franz J., Jaouen, Etienne, Möckel, Martin M., Rühle, Frank, Butter, Falk, Basilicata, M. Felicia, Keller Valsecchi, Claudia Isabelle
Format: Article
Language:English
Subjects:
Alternative splicing
Anopheles
Biological evolution
Chromosomes
Compensation
Culicidae
DNA-binding protein
Dosage
Dosage compensation
Females
Gender differences
Gene expression
Genes
Insects
Life Sciences
Malaria
Males
Mosquitoes
Peptides
Proteins
Sex chromosomes
Sex differentiation
Sexes
Vector-borne diseases
X chromosomes
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Summary: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 unresolved 1 . 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.
ISSN:0028-0836
1476-4687
DOI:10.1038/s41586-023-06641-0