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Cerebellar cortical lamination and foliation require cyclin A2

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Cerebellar cortical lamination and foliation require cyclin A2. / Otero, José Javier; Kalaszczynska, Ilona; Michowski, Wojciech; Wong, Michael; Gygli, Patrick Edwin; Gokozan, Hamza Numan; Griveau, Amélie; Odajima, Junko; Czeisler, Catherine; Catacutan, Fay Patsy; Murnen, Alice; Schüller, Ulrich; Sicinski, Piotr; Rowitch, David H.

in: DEV BIOL, Jahrgang 385, Nr. 2, 15.01.2014, S. 328-39.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Otero, JJ, Kalaszczynska, I, Michowski, W, Wong, M, Gygli, PE, Gokozan, HN, Griveau, A, Odajima, J, Czeisler, C, Catacutan, FP, Murnen, A, Schüller, U, Sicinski, P & Rowitch, DH 2014, 'Cerebellar cortical lamination and foliation require cyclin A2', DEV BIOL, Jg. 385, Nr. 2, S. 328-39. https://doi.org/10.1016/j.ydbio.2013.10.019

APA

Otero, J. J., Kalaszczynska, I., Michowski, W., Wong, M., Gygli, P. E., Gokozan, H. N., Griveau, A., Odajima, J., Czeisler, C., Catacutan, F. P., Murnen, A., Schüller, U., Sicinski, P., & Rowitch, D. H. (2014). Cerebellar cortical lamination and foliation require cyclin A2. DEV BIOL, 385(2), 328-39. https://doi.org/10.1016/j.ydbio.2013.10.019

Vancouver

Otero JJ, Kalaszczynska I, Michowski W, Wong M, Gygli PE, Gokozan HN et al. Cerebellar cortical lamination and foliation require cyclin A2. DEV BIOL. 2014 Jan 15;385(2):328-39. https://doi.org/10.1016/j.ydbio.2013.10.019

Bibtex

@article{fd371c9e8b2b41e5b9df96d33b917c17,
title = "Cerebellar cortical lamination and foliation require cyclin A2",
abstract = "The mammalian genome encodes two A-type cyclins, which are considered potentially redundant yet essential regulators of the cell cycle. Here, we tested requirements for cyclin A1 and cyclin A2 function in cerebellar development. Compound conditional loss of cyclin A1/A2 in neural progenitors resulted in severe cerebellar hypoplasia, decreased proliferation of cerebellar granule neuron progenitors (CGNP), and Purkinje (PC) neuron dyslamination. Deletion of cyclin A2 alone showed an identical phenotype, demonstrating that cyclin A1 does not compensate for cyclin A2 loss in neural progenitors. Cyclin A2 loss lead to increased apoptosis at early embryonic time points but not at post-natal time points. In contrast, neural progenitors of the VZ/SVZ did not undergo increased apoptosis, indicating that VZ/SVZ-derived and rhombic lip-derived progenitor cells show differential requirements to cyclin A2. Conditional knockout of cyclin A2 or the SHH proliferative target Nmyc in CGNP also resulted in PC neuron dyslamination. Although cyclin E1 has been reported to compensate for cyclin A2 function in fibroblasts and is upregulated in cyclin A2 null cerebella, cyclin E1 expression was unable to compensate for loss-of cyclin A2 function.",
keywords = "Animals, Cell Proliferation, Cerebral Cortex, Cyclin A2, In Situ Hybridization, Mice, Mice, Knockout, Mice, Transgenic, Neural Stem Cells, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Otero, {Jos{\'e} Javier} and Ilona Kalaszczynska and Wojciech Michowski and Michael Wong and Gygli, {Patrick Edwin} and Gokozan, {Hamza Numan} and Am{\'e}lie Griveau and Junko Odajima and Catherine Czeisler and Catacutan, {Fay Patsy} and Alice Murnen and Ulrich Sch{\"u}ller and Piotr Sicinski and Rowitch, {David H}",
note = "{\textcopyright} 2013 Elsevier Inc. All rights reserved.",
year = "2014",
month = jan,
day = "15",
doi = "10.1016/j.ydbio.2013.10.019",
language = "English",
volume = "385",
pages = "328--39",
journal = "DEV BIOL",
issn = "0012-1606",
publisher = "Academic Press Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Cerebellar cortical lamination and foliation require cyclin A2

AU - Otero, José Javier

AU - Kalaszczynska, Ilona

AU - Michowski, Wojciech

AU - Wong, Michael

AU - Gygli, Patrick Edwin

AU - Gokozan, Hamza Numan

AU - Griveau, Amélie

AU - Odajima, Junko

AU - Czeisler, Catherine

AU - Catacutan, Fay Patsy

AU - Murnen, Alice

AU - Schüller, Ulrich

AU - Sicinski, Piotr

AU - Rowitch, David H

N1 - © 2013 Elsevier Inc. All rights reserved.

PY - 2014/1/15

Y1 - 2014/1/15

N2 - The mammalian genome encodes two A-type cyclins, which are considered potentially redundant yet essential regulators of the cell cycle. Here, we tested requirements for cyclin A1 and cyclin A2 function in cerebellar development. Compound conditional loss of cyclin A1/A2 in neural progenitors resulted in severe cerebellar hypoplasia, decreased proliferation of cerebellar granule neuron progenitors (CGNP), and Purkinje (PC) neuron dyslamination. Deletion of cyclin A2 alone showed an identical phenotype, demonstrating that cyclin A1 does not compensate for cyclin A2 loss in neural progenitors. Cyclin A2 loss lead to increased apoptosis at early embryonic time points but not at post-natal time points. In contrast, neural progenitors of the VZ/SVZ did not undergo increased apoptosis, indicating that VZ/SVZ-derived and rhombic lip-derived progenitor cells show differential requirements to cyclin A2. Conditional knockout of cyclin A2 or the SHH proliferative target Nmyc in CGNP also resulted in PC neuron dyslamination. Although cyclin E1 has been reported to compensate for cyclin A2 function in fibroblasts and is upregulated in cyclin A2 null cerebella, cyclin E1 expression was unable to compensate for loss-of cyclin A2 function.

AB - The mammalian genome encodes two A-type cyclins, which are considered potentially redundant yet essential regulators of the cell cycle. Here, we tested requirements for cyclin A1 and cyclin A2 function in cerebellar development. Compound conditional loss of cyclin A1/A2 in neural progenitors resulted in severe cerebellar hypoplasia, decreased proliferation of cerebellar granule neuron progenitors (CGNP), and Purkinje (PC) neuron dyslamination. Deletion of cyclin A2 alone showed an identical phenotype, demonstrating that cyclin A1 does not compensate for cyclin A2 loss in neural progenitors. Cyclin A2 loss lead to increased apoptosis at early embryonic time points but not at post-natal time points. In contrast, neural progenitors of the VZ/SVZ did not undergo increased apoptosis, indicating that VZ/SVZ-derived and rhombic lip-derived progenitor cells show differential requirements to cyclin A2. Conditional knockout of cyclin A2 or the SHH proliferative target Nmyc in CGNP also resulted in PC neuron dyslamination. Although cyclin E1 has been reported to compensate for cyclin A2 function in fibroblasts and is upregulated in cyclin A2 null cerebella, cyclin E1 expression was unable to compensate for loss-of cyclin A2 function.

KW - Animals

KW - Cell Proliferation

KW - Cerebral Cortex

KW - Cyclin A2

KW - In Situ Hybridization

KW - Mice

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Neural Stem Cells

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.ydbio.2013.10.019

DO - 10.1016/j.ydbio.2013.10.019

M3 - SCORING: Journal article

C2 - 24184637

VL - 385

SP - 328

EP - 339

JO - DEV BIOL

JF - DEV BIOL

SN - 0012-1606

IS - 2

ER -