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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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Partnership

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 CRISPR-KissCas9 project word cloud

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

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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