2018
HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals
VEČEŘA, Josef, Eva BÁRTOVÁ, Jana KREJČÍ, Soňa LEGARTOVÁ, Denisa KOMŮRKOVÁ et. al.Základní údaje
Originální název
HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals
Autoři
VEČEŘA, Josef (203 Česká republika, domácí), Eva BÁRTOVÁ (203 Česká republika, garant), Jana KREJČÍ (203 Česká republika), Soňa LEGARTOVÁ (703 Slovensko), Denisa KOMŮRKOVÁ (203 Česká republika), Jana RUDÁ (203 Česká republika, domácí), Tibor ŠTARK (703 Slovensko, domácí), Eva DRAŽANOVÁ (203 Česká republika, domácí), Tomáš KAŠPÁREK (203 Česká republika, domácí), Alexandra ŠULCOVÁ (203 Česká republika, domácí), Frank J. DEKKER (528 Nizozemské království), Wiktor SZYMANSKI (528 Nizozemské království), Christian SEISER (40 Rakousko), Georg WEITZER (40 Rakousko), Raphael MECHOULAM (376 Izrael), Vincenzo MICALE (380 Itálie, domácí) a Stanislav KOZUBEK (203 Česká republika, domácí)
Vydání
Journal of cellular physiology, United States, Wiley-Liss, 2018, 0021-9541
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30105 Physiology
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 4.522
Kód RIV
RIV/00216224:14110/18:00100736
Organizační jednotka
Lékařská fakulta
UT WoS
000411829600046
Klíčová slova anglicky
acetylome; H3K9 acetylation; HDACs; mouse neurogenesis; schizophrenia
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 23. 4. 2024 09:55, Mgr. Michal Petr
Anotace
V originále
Although histone acetylation is one of the most widely studied epigenetic modifications, there is still a lack of information regarding how the acetylome is regulated during brain development and pathophysiological processes. We demonstrate that the embryonic brain (E15) is characterized by an increase in H3K9 acetylation as well as decreases in the levels of HDAC1 and HDAC3. Moreover, experimental induction of H3K9 hyperacetylation led to the overexpression of NCAM in the embryonic cortex and depletion of Sox2 in the subventricular ependyma, which mimicked the differentiation processes. Inducing differentiation in HDAC1-deficient mouse ESCs resulted in early H3K9 deacetylation, Sox2 downregulation, and enhanced astrogliogenesis, whereas neuro-differentiation was almost suppressed. Neuro-differentiation of (wt) ESCs was characterized by H3K9 hyperacetylation that was associated with HDAC1 and HDAC3 depletion. Conversely, the hippocampi of schizophrenia-like animals showed H3K9 deacetylation that was regulated by an increase in both HDAC1 and HDAC3. The hippocampi of schizophrenia-like brains that were treated with the cannabinoid receptor-1 inverse antagonist AM251 expressed H3K9ac at the level observed in normal brains. Together, the results indicate that co-regulation of H3K9ac by HDAC1 and HDAC3 is important to both embryonic brain development and neuro-differentiation as well as the pathophysiology of a schizophrenia-like phenotype.
Návaznosti
GBP302/12/G157, projekt VaV |
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GJ15-13443Y, projekt VaV |
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LQ1601, projekt VaV |
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3SGA5789, interní kód MU |
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