DYRK1A promotes dopaminergic neuron survival in the developing brain and in a mouse model of Parkinson's disease
Identifieur interne : 000A21 ( Main/Exploration ); précédent : 000A20; suivant : 000A22DYRK1A promotes dopaminergic neuron survival in the developing brain and in a mouse model of Parkinson's disease
Auteurs : M J Barallobre [Espagne] ; C. Perier [Espagne] ; J. Bové [Espagne] ; A. Laguna [Espagne] ; J M Delabar [France] ; M. Vila [Espagne] ; M L Arbonés [Espagne]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2014.
Abstract
In the brain, programmed cell death (PCD) serves to adjust the numbers of the different types of neurons during development, and its pathological reactivation in the adult leads to neurodegeneration. Dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A) is a pleiotropic kinase involved in neural proliferation and cell death, and its role during brain growth is evolutionarily conserved. Human
Url:
DOI: 10.1038/cddis.2014.253
PubMed: 24922073
PubMed Central: 4611726
Affiliations:
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, Barcelona,<country>Spain</country>
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, Barcelona,<country>Spain</country>
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<front><div type="abstract" xml:lang="en"><p>In the brain, programmed cell death (PCD) serves to adjust the numbers of the different types of neurons during development, and its pathological reactivation in the adult leads to neurodegeneration. Dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A) is a pleiotropic kinase involved in neural proliferation and cell death, and its role during brain growth is evolutionarily conserved. Human <italic>DYRK1A</italic>
lies in the Down syndrome critical region on chromosome 21, and heterozygous mutations in the gene cause microcephaly and neurological dysfunction. The mouse model for <italic>DYRK1A</italic>
haploinsufficiency (the <italic>Dyrk1a</italic>
<sup>+/−</sup>
mouse) presents neuronal deficits in specific regions of the adult brain, including the substantia nigra (SN), although the mechanisms underlying these pathogenic effects remain unclear. Here we study the effect of <italic>DYRK1A</italic>
copy number variation on dopaminergic cell homeostasis. We show that mesencephalic DA (mDA) neurons are generated in the embryo at normal rates in the <italic>Dyrk1a</italic>
haploinsufficient model and in a model (the mBACtg<italic>Dyrk1a</italic>
mouse) that carries three copies of <italic>Dyrk1a</italic>
. We also show that the number of mDA cells diminishes in postnatal <italic>Dyrk1a</italic>
<sup>+/−</sup>
mice and increases in mBACtg<italic>Dyrk1a</italic>
mice due to an abnormal activity of the mitochondrial caspase9 (Casp9)-dependent apoptotic pathway during the main wave of PCD that affects these neurons. In addition, we show that the cell death induced by 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP), a toxin that activates Casp9-dependent apoptosis in mDA neurons, is attenuated in adult mBACtg<italic>Dyrk1a</italic>
mice, leading to an increased survival of SN DA neurons 21 days after MPTP intoxication. Finally, we present data indicating that Dyrk1a phosphorylation of Casp9 at the Thr125 residue is the mechanism by which this kinase hinders both physiological and pathological PCD in mDA neurons. These data provide new insight into the mechanisms that control cell death in brain DA neurons and they show that deregulation of developmental apoptosis may contribute to the phenotype of patients with imbalanced <italic>DYRK1A</italic>
gene dosage.</p>
</div>
</front>
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<affiliations><list><country><li>Espagne</li>
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