Marie Skłodowska-Curie Actions

Post-doctoral Research Fellowship: MSCA-IF 2017 at the Department of Physiology

    01/09/2018 12:30 - Europe/Brussels
    H2020 / Marie Skłodowska-Curie Actions
    Spain, Granada
    International Project Office
    Promotion & Advisory Unit

Professor Darío Acuña Castroviejo, from the Department of Physiology at the University of Granada, welcomes postdoctoral candidates interested in applying for a Marie Skłodowska-Curie Individual Fellowships (MSCA-IF) in this university. Applicants must comply with the Mobility Rule (more information in the participant guide: http://sl.ugr.es/097k).

Darío Acuña-Castroviejo is responsible for the research group CTS-101: Intercellular Communication. This group has been constituted in 1988 and it is devoted to the study of melatonin-mitochondria interaction in health and disease. We also work analysing natural products of microbial sources as antioxidant and anti-inflammatory looking for their clinical application. Specifically, the group is working on experimental models of aging, sepsis, Parkinson’s disease, and cancer. Models include cell culture, zebrafish, mice, and rat. We analyse the inflammatory pathways, oxidative stress pathways, nucleus-mitochondria connection, mitochondrial pathways of cell death, mitochondrial dynamic, clock genes and clock-controlled genes, mTOR pathways, etc. One of the models that we are currently working is on the zebrafish mutants with the CRISP/Cas9 methodology. We use MR and in vivo spectroscopy, in vivo luminescence to check the expression of some genes; high resolution respirometry in vivo, permeabilized muscle fibres and in isolated mitochondria; UPLC-mass spectrometry; qRT-PCR; NB, WB; mutagenesis; HPLC, fluorometry, etc. Some of the results of our experiments have been patented and three of them transfer to the pharmaceutical industry, with two clinical trials currently performing. Moreover, we have two biotechnological Spin-offs devoted to the development of some of these patents.

The first studies conducted to assess the melatonin roles were done in pinealectomized animals, leading to identify the participation of the indoleamine in the regulation of circadian rhythms. Pinealectomy, however, did not seem to produced important effects due to the lack of melatonin, understimating its role in both animal and human physiology. After the discovery that melatonin is sinthetized in almost every organ and tissue of the body, it became clear that pinealectomy does not produce a whole melatonin deficit and, thus, not severe alterations could appear after pinealectomy. The important effects due to extrapineal melatonin elsewhere reported, as so as its clinical applications, support a main role in the organism’s homeostasis for the indoleamine. To date, the attempts to obtain a full melatonin-deficient mouse model have clearly failed, because of the difficulty to blunt the asmt (acetylserotonin-N-methyltransferase) gene, which codes for asmt, the last enzyme in the melatonin synthesis. The main objective of this project is to generate a whole melatonin deficient zebrafish model, which have two genes codding for asmt (1 and 2) that have been sequenced, with the CRISPR/Cas9 technical approach. In this melatonin-deficient zebrafish model it will be evaluated: 1) its viability; otherwise we will use heterocygotes; 2) development, with particular emphasis on macro and microsocopical malformations, breeding and laying up to the adult age of 3-4 months; 3) circadian rhythms (sleep/wake, feeding, locomotor activity, clock genes expression); 4) mitochondrial function along the development; 5) genomic and  proteomic analysis to identify impaired pathways, and 6) to analyze these changes after melatonin treatment to the mutant zebrafish.

Research Area:

  • Life Sciences (LIF)

For a correct evaluation of your candidature, please send the documents below to Professor (dacuna@ugr.es):

  • CV
  • Letter of recommendation (optional)