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Kerimoglu, C.* ; Pham, L.* ; Tonchev, A.B.* ; Sakib, M.S.* ; Xie, Y.* ; Sokpor, G.* ; Ulmke, P.A.* ; Kaurani, L.* ; Abbas, E.* ; Nguyen, H.T.* ; Rosenbusch, J.* ; Michurina, A.* ; Capece, V.* ; Angelova, M.* ; Maricic, N.* ; Brand-Saberi, B.* ; Esgleas Izquierdo, M. ; Albert, M.* ; Minkov, R.* ; Kovachev, E.* ; Teichmann, U.* ; Seong, R.H.* ; Huttner, W.B.* ; Nguyen, H.P.* ; Stoykova, A.* ; Staiger, J.F.* ; Fischer, A.* ; Tuoc, T.*

H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion.

Sci. Adv. 7:eabc6792 (2021)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag

Increase in the size of human neocortex―acquired in evolution―accounts for the unique cognitive capacity of humans. This expansion reflects the evolutionarily enhanced proliferative ability of basal progenitors (BPs), including the basal radial glia and basal intermediate progenitors (bIPs) in mammalian cortex, which may have been acquired through epigenetic alterations in BPs. However, how the epigenome in BPs differs across species is not known. Here, we report that histone H3 acetylation is a key epigenetic regulation in bIP amplification and cortical expansion. Through epigenetic profiling of sorted bIPs, we show that histone H3 lysine 9 acetylation (H3K9ac) is low in murine bIPs and high in human bIPs. Elevated H3K9ac preferentially increases bIP proliferation, increasing the size and folding of the normally smooth mouse neocortex. H3K9ac drives bIP amplification by increasing expression of the evolutionarily regulated gene, Trnp1, in developing cortex. Our findings demonstrate a previously unknown mechanism that controls cortical architecture.

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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Outer Subventricular Zone; Cerebral Cortical Size; Radial Glia; Lissencephalic Primate; Germinal Zones; Cell; Cortex; Pax6; Neurogenesis; Evolution
ISSN (print) / ISBN 2375-2548
e-ISSN 2375-2548
Zeitschrift Science Advances
Quellenangaben Band: 7, Heft: 38, Seiten: , Artikelnummer: eabc6792 Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Verlagsort Washington, DC [u.a.]
Begutachtungsstatus Peer reviewed