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CRISPR-KissCas9 SIGNED

Challenging the KNDy Hypothesis Using CRISPR-Cas9 Genome Editing: Evaluation of the Role of Neurokinin B and Dynorphin in Kiss1 neurons in the Control of Fertility

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EC-Contrib. €

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 CRISPR-KissCas9 project word cloud

Explore the words cloud of the CRISPR-KissCas9 project. It provides you a very rough idea of what is the project "CRISPR-KissCas9" about.

signaling    hormone    ovarian    population    co    reciprocal    dependent    synthesizes    mechanisms    secretion    editing    syndrome    neurokinin    neuroendocrine    neuropeptides    dyn    lh    aid    first    treat    fertility    release    dynamic    name    clarified    gonadotropin    interplay    kisspeptins    genome    physiological    function    inhibitory    neurons    pcos    neurosecretion    polycystic    respectively    play    outlined    axis    hypogonadism    functional    alterations    models    relevance    expresses    coined    roles    kndy    nkb    reproductive    tools    dependence    substantially    pulse    neuronal    mouse    dynorphin    networks    loci    kiss1    cas9    pointed    gonadal    basic    pituitary    regulation    regulates    pdyn    mastered    gnrh    nucleus    patho    kp    output    subfertility    virogenetic    time    fsh    seemingly    gene    crispr    genetic    hpg    hypothalamic    stimulatory    encoded    disorders    perturbations    arc    generation    tac2    somatic    suitable    producing    metabolic    arcuate    strategies    releasing    abnormalities    pulsatile   

Project "CRISPR-KissCas9" data sheet

The following table provides information about the project.

Coordinator		 UNIVERSIDAD DE CORDOBA 

Organization address
address: AVENIDA DE MEDINA AZAHARA 5
city: CORDOBA
postcode: 14005
website: www.uco.es

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.
 Coordinator Country Spain [ES]
 Total cost 160˙932 €
 EC max contribution 160˙932 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2022-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSIDAD DE CORDOBA ES (CORDOBA) coordinator 160˙932.00

Map

 Project objective

The function of the hypothalamic-pituitary-gonadal (HPG) axis is mastered by the hypothalamic neuronal population producing gonadotropin-releasing hormone (GnRH), which regulates LH and FSH secretion by the pituitary. Perturbations of fertility, e.g., in polycystic ovarian syndrome (PCOS) and hypogonadism associated with metabolic disorders, are related to functional alterations in the neuronal networks controlling pulsatile GnRH secretion. Recently, a neuronal population in the hypothalamic arcuate nucleus (ARC), which synthesizes kisspeptins (Kp; products of the Kiss1 gene), has been identified as an essential element in the regulation of pulsatile GnRH release. This ARC Kiss1 neuronal population co-expresses the neuropeptides, neurokinin B (NKB; encoded by Tac2) and dynorphin-A (Dyn; encoded by Pdyn); the term KNDy (for Kiss1, NKB & Dyn) has been coined to name this population. Different studies have pointed out the reciprocal stimulatory and inhibitory roles of NKB and Dyn, respectively, in the control of Kp output, which seemingly play a crucial role in the control of GnRH pulse generation. However, the relevance of such NKB/Dyn interplay in the dynamic control of GnRH release in different (patho)-physiological conditions, and whether this is fully dependent on Kp signaling, has not been fully clarified. We propose here to apply for the first time somatic genome editing of Tac2, Pdyn and Kiss1 loci in KNDy neurons, by using the CRISPR/Cas9 technology and virogenetic tools in suitable genetic mouse models, to address the physiological roles of NKB and Dyn in the dynamic control of GnRH neurosecretion, and their dependence on Kp signaling. The studies outlined in this proposal will substantially advance our understanding of basic neuroendocrine mechanisms for the control of fertility and will aid for the development of better strategies to treat reproductive abnormalities, such as polycystic ovarian syndrome and in/ subfertility related to metabolic disorders.

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The information about "CRISPR-KISSCAS9" are provided by the European Opendata Portal: CORDIS opendata.

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