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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

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

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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