Abstract
Neuronal and glial progenitor cells exist in the adult Drosophila brain. The primarily glial progenitor cells rely on a microRNA, mir-31a, to inhibit the expression of a predicted E3 ubiquitin ligase, CG16947. Erroneous inheritance of CG16947 by the progeny when the neural progenitor cell divides leads to death of the progeny, however how CG16947 achieves glial cell death is unknown. I have identified the interacting partner of CG16947 to be cdk9. I show that reduction of cdk9 expression in glia causes glial loss; highlighting the importance of cdk9 in mediating the survival of glia. Further, glial loss observed in mir-31a mutants was prevented with adult-specific expression of cdk9 in glia. I provide biochemical evidence that the binding of CG16947 to cdk9 causes its degradation. Taken together, this data shows that cdk9 plays a role in the survival of adult glia in the Drosophila brain. Thus, a fine balance exists between mir-31a and CG16947 expression in the progenitor cells that in turn regulates the levels of cdk9 in the progeny. This serves to allow the progenitor cells to regulate the number of glia in the adult brain.
Highlights
The study of glial production in the adult has largely centred on aberrant glial division in injury or in disease states such as in the formation of glioblastoma
I show that the expression of cdk[9] in adult glia can prevent the glial loss observed in mir-31a mutants
CG16947 expression in a subset of progenitor cells in the adult brain is controlled by the microRNA, mir-31a
Summary
The study of glial production in the adult has largely centred on aberrant glial division in injury or in disease states such as in the formation of glioblastoma. In mir-31a mutants, where the inhibition of CG16947 translation is lifted by the absence of mir-31a, there is excessive expression of CG16947 in the progenitor cells This leads to aberrant inheritance of CG16947 by the glial progeny, leading to their death by apoptosis[4]. I show that the expression of cdk[9] in adult glia can prevent the glial loss observed in mir-31a mutants. Taken together, this data shows that cdk[9] mediates the survival of glia in the adult Drosophila brain
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