• Keywords

synaptic plasticity, autism spectrum disorder, Immediate early genes, behaviour, antibody fragment

• Profile and skills required

The applicant must have a Master degree (or equivalent) in biology. Strong knowledge in cellular or molecular biology and/or Neurosciences is required, with excellent oral and writing skills in English (mandatory) to present in national and international meetings and to write research articles in scientific journals. Knowledge in antibody display or virology would be advantageous.

We are seeking for a dynamic person who will be able to fully commit in his PhD project, propose new ideas, be curious, with a critical mind, display some autonomy and would be willing to learn new skills.

To apply for the position, please provide a detailed resume (university, formations, skills, internships, the name of two references), a motivation letter (one page), and a summary (one page) and grades of the Master.

• Project description

Studies have revealed common global dysregulation in synaptic transmission and plasticity in ASD patients and animal models, notably in the striatum In ASD patients and animal models of the disorder (1, 2). Immediate early genes control synaptic plasticity in response to various external stimuli. Within minutes, they are transcribed, transported to dendrites and locally translated in proteins. Therefore, we hypothesized that these genes could be involved in the synaptic plasticity underpinning social behaviors (3). Furthermore, one of these genes has been shown to be able to transport mRNA to neighboring neurons in neuronal culture and at the neuromuscular junction of drosophila (4, 5). Until now, their role in the control of social behavior remains unknown. The objectives of the PhD projects are 1) identifying the effect of different social stimuli on neuronal plasticity markers in WT and social interaction deficit mouse models, 2) studying the activity of these markers in the control of social behaviors, 3) testing in vivo their use to improve social skills in mouse models of ASD.

• References

1. Neuhaus, E., T.P. Beauchaine, and R. Bernier, Neurobiological correlates of social functioning in autism. Clin Psychol Rev, 2010. 30(6): p. 733-48.

2. Bourgeron, T., From the genetic architecture to synaptic plasticity in autism spectrum disorder. Nat Rev Neurosci, 2015. 16(9): p. 551-63.

3. Wang, K.H., et al., In vivo two-photon imaging reveals a role of arc in enhancing orientation specificity in visual cortex. Cell, 2006. 126(2): p. 389-402.

4. Ashley, J., et al., Retrovirus-like Gag Protein Arc1 Binds RNA and Traffics across Synaptic Boutons. Cell, 2018. 172(1-2): p. 262-274 e11.

5. Pastuzyn, E.D., et al., The Neuronal Gene Arc Encodes a Repurposed Retrotransposon Gag Protein that Mediates Intercellular RNA Transfer. Cell, 2018. 172(1-2): p. 275-288 e18.

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