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

Archive ouverte

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

Edité par CCSD ; Nature Publishing Group -

International audience. 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.

• Description
• Sujet/Public
• Outil
• Outil d'anticipation
• Mémoire et thèse
• Gestion