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One of the greatest challenges in neuroscience is to understand how a complex structure, such as the brain, is built. Spatial and temporal patternings of neuronal progenitors are responsible for the generation of most of the neuronal diversity observed in the brain. This review focuses on the temporal patterning of neuronal progenitors, i.e. the sequential expression of transcription factors that changes the capacity of stem cells to generate different neuronal types, and which is conserved in animals. Recent papers have offered a near complete understanding of the mechanism of temporal patterning in the developing visual system of Drosophila, and of how this contributes to the specification of diverse neuronal identities, which are then maintained by the sustained expression of downstream transcription factors. The insect visual system provides a unique model to study the evolution of neuronal cell types, as well as the evolution of neurodevelopmental mechanisms that generate them., (© 2024 médecine/sciences – Inserm.)

Traditionally, mRNA decay was considered a simple destruction step of mRNA. This view has been challenged in the past years and mRNA decay now appears as an essential step in the regulation of gene expression. We first present a short review of the different reactions involved in mRNA decay, as well as some indications on their cellular location. Then, we describe two processes in which mRNA decay plays an essential role: (1) the mRNA quality control mechanisms that get rid of aberrant mRNAs (nonsensE-mediated decay, non-stop decay, no-go decay); (2) the regulation of mRNA stability through the targeting of specific factors to the mRNA (proteins or small non-coding RNAs).

Huntington's disease is an hereditary dominant neurodegenerative disorder clinically characterised by progressive motor deficits, personality changes, decreased mental capacity and death after about 15-20 years. Most studies are based on the research of intrinsic mechanisms that could be responsible for dysfunction and later degeneration of neuronal subsets. It is only in the last five years that more interest has been focused on another brain cell type : the astrocytes. This review presents evidence that astroglial function is also affected in Huntington's disease. Among the possible mechanisms, Huntington's disease mutation may alter the EGF receptor signaling pathway, that regulates the astrocytic response to neuronal injuries.

Given alone to Drosophila adults, casein is almost not used because it is not ingested. L arabinose, which is a powerful phagostimulant allows a convenient utilisation of casein, resulting in an increase of life duration and egg production. The utilisation is still improved when a small amount of alcohol is added. Ethanol acts both as an energy source and as a phagostimulant.

14C-adenosine is incorporated very little inot nucleic acids of Drosophila cells cultured in a medium free of foetal calf serum. The greater part of the radioactivity is recovered in inosine and hypoxanthine. These results suggest that the principal pathway of ultilization of adenosine is not mediated by adenosine kinase. Adenosine is rapidly deaminated to inosine by adenosine deaminase, and cleaved to hypoxanthine by inosine phosphorylase. Inosine and hypoxanthine not being substrates for Drosophila cell lines, are released into the culture medium.

At 25 degrees C, mean survival duration of adults starved after emergence varied from 58 to 112 hours, according to genotype and larval growth conditions. This duration was highly correlated with the amount of lipids. The great variability in the amount of lipids (from 15 to 35% of initial dry weight) seems to have an adaptative significance for adult survival in natural conditions.