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