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Fabre, C. C. G.

Publications and source records attributed to Fabre, C. C. G..

2 recordsLinked to original sources

Drosophila males require the longitudinal stretch receptors to tremulate their abdomen and produce substrate-borne signals during courtship

Substrate-borne cues are important species-specific signals that are widely used during courtship of many animals, from arthropods to vertebrates. They allow mating partners to communicate with, recognise and choose one another. Animals often produce substrate-borne signals by vibrating a body part, such as the abdomen. During Drosophila courtship, species-specific substrate-borne vibrations are generated by the males regular up-and-down abdominal tremulations and these must be precisely controlled to produce an effective and specific signal. The vibrations immobilise the female, therefore facilitating copulation. It is not known how the males nervous system regulates this abdominal tremulation. Here, we demonstrate a role for the dorsal abdominal longitudinal stretch receptors (LSR), which include the dorsal bipolar dendritic (dbd) neurons. These neurons are a set of conserved proprioceptors found throughout Insecta. We show that impairing the function of dbd neurons through general inhibition results in males exhibiting high level of arhythmic abdominal movements (referred to as bobbing) and decreased level of tremulation. Strikingly, this causes a failure in the females response during courtship. We show that depleting the mechanosensitive ion channel TRPA1 (but not Piezo) in the dbd neurons leads to a similar increase in bobbing movements. Thus, we identify neurons and a key molecular player necessary for males to perform this important mode of communication.

neuroscience↗

Essential conserved neuronal motors kinesin-1 and kinesin-3 regulate Abeta42 toxicity in vivo

Alzheimers Disease is the leading cause of dementia and the most common neurodegenerative disorder. Understanding the molecular pathology of Alzheimers Disease may help identify new ways to reduce neuronal damage. In the past decades Drosophila has become a powerful tool in modelling mechanisms underlying human diseases. Here we investigate how the expression of the human 42-residue {beta}-amyloid (A{beta}) carrying the E22G pathogenic "Arctic" mutation (A{beta}42Arc) affects axonal health and behaviour of Drosophila. We find that A{beta}42Arc flies present aberrant neurons, with altered axonal transport of mitochondrial and an increased number of terminal boutons at neuromuscular junctions. We demonstrate that the major axonal motor proteins kinesin-1 and kinesin-3 are essential for the correct development of neurons in Drosophila larvae and similar findings are replicated in human iPSC-derived cortical neurons. We then show that the over-expression of kinesin-1 or kinesin-3 restores the correct number of terminal boutons in A{beta}42Arc expressing neurons and that this is associated with a rescue of the overall neuronal function, measured by negative geotaxis locomotor behavioural assay. We therefore provide new evidence in understanding the mechanisms of axonal transport defects in Alzheimers Disease, and our results indicate that kinesins should be considered as potential drug targets to help reduce dementia-associated disorders.

cell biology↗