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

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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