| Autor: |
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 |
| Zdroj: |
Nature; Nov2023, Vol. 623 Issue 7985, p175-182, 8p |
| Abstrakt: |
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.A newly identified gene, sex chromosome activation (SOA), is a master regulator of dosage compensation in Anopheles gambiae. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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