Injury or trauma to the brain causes damage to the nervous system and can trigger an immune response. The ability of neurons to repair damage has long been known to depend both on their intrinsic properties and on extrinsic factors, in particular, the immune system. Over the last decade, the nematode C. elegans has emerged as an extremely powerful genetic model organism for immunologists and neurobiologists to discover evolutionary conserved mechanisms. Dr. Yishi Jin’s lab at University of California, San Diego (UCSD), has pioneered the use of C. elegans to examine genetic factors underlying axonal injury responses. Their work has identified multiple regulators that act primarily in the injured neurons to initiate axon regrowth, one of them being a transcription factor known as CEBP-1. Independently, Drs. Nathalie Pujol and Jonathan Ewbank at CIML (AMU) have investigated the pathways underlying the innate

immunity of C. elegans to fungal infection. They have studied genes that act primarily in the epidermis, one being a conserved kinase Tribbles/NIPI-3. Interestingly, they identified CEBP-1 as an interactor of NIPI-3. The purpose of this IMéRA proposal is to enable Dr. Jin to explore common signaling modules shared between the nervous system and the epidermis, with the following specific goals: First, to complete an on-going inter-disciplinary collaborative study on the interaction of CEBP-1 and NIPI-3 in neurons and in epidermis. Second, to establish new strategies exploring the crosstalk between immunity and neural trauma. Third, to facilitate scientific exchange and forge collaborations between UCSD and AMU through participation in the IMéRA scholar program.