The loss of the kinases SadA and SadB results in early neuronal apoptosis and a reduced number of progenitors
The neurons that form the mammalian neocortex originate from progenitor cells in the ventricular (VZ) and subventricular zone (SVZ). Newborn neurons are multipolar but become bipolar during their migration from the germinal layers to the cortical plate (CP) by forming a leading process and an axon t...
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| creator | Dhumale, Pratibha Menon, Sindhu Chiang, Joanna Püschel, Andreas W |
| description | The neurons that form the mammalian neocortex originate from progenitor cells in the ventricular (VZ) and subventricular zone (SVZ). Newborn neurons are multipolar but become bipolar during their migration from the germinal layers to the cortical plate (CP) by forming a leading process and an axon that extends in the intermediate zone (IZ). Once they settle in the CP, neurons assume a highly polarized morphology with a single axon and multiple dendrites. The AMPK-related kinases SadA and SadB are intrinsic factors that are essential for axon formation during neuronal development downstream of Lkb1. The knockout of both genes encoding Sad kinases (Sada and Sadb) results not only in a loss of axons but also a decrease in the size of the cortical plate. The defect in axon formation has been linked to a function of Sad kinases in the regulation of microtubule binding proteins. However, the causes for the reduced size of the cortical plate in the Sada-/-;Sadb-/- knockout remain to be analyzed in detail. Here we show that neuronal cell death is increased and the number of neural progenitors is decreased in the Sada-/-;Sadb-/- CP. The reduced number of progenitors is a non-cell autonomous defect since they do not express Sad kinases. These defects are restricted to the neocortex while the hippocampus remains unaffected. |
| doi_str_mv | 10.1371/journal.pone.0196698 |
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Newborn neurons are multipolar but become bipolar during their migration from the germinal layers to the cortical plate (CP) by forming a leading process and an axon that extends in the intermediate zone (IZ). Once they settle in the CP, neurons assume a highly polarized morphology with a single axon and multiple dendrites. The AMPK-related kinases SadA and SadB are intrinsic factors that are essential for axon formation during neuronal development downstream of Lkb1. The knockout of both genes encoding Sad kinases (Sada and Sadb) results not only in a loss of axons but also a decrease in the size of the cortical plate. The defect in axon formation has been linked to a function of Sad kinases in the regulation of microtubule binding proteins. However, the causes for the reduced size of the cortical plate in the Sada-/-;Sadb-/- knockout remain to be analyzed in detail. Here we show that neuronal cell death is increased and the number of neural progenitors is decreased in the Sada-/-;Sadb-/- CP. The reduced number of progenitors is a non-cell autonomous defect since they do not express Sad kinases. These defects are restricted to the neocortex while the hippocampus remains unaffected.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0196698</identifier><identifier>PMID: 29698519</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alzheimer's disease ; Apoptosis ; Axonogenesis ; Axons ; Biology and Life Sciences ; Brain research ; Cell cycle ; Cell death ; Cells (biology) ; Defects ; Dendrites ; Feedback ; Genotype & phenotype ; Kinases ; LKB1 protein ; Mammals ; Medicine and Health Sciences ; Morphology ; Neocortex ; Neural stem cells ; Neurons ; Progenitor cells ; Protein binding ; Proteins ; Research and Analysis Methods ; Rodents ; Subventricular zone ; Ventricle</subject><ispartof>PloS one, 2018-04, Vol.13 (4), p.e0196698-e0196698</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Dhumale et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Newborn neurons are multipolar but become bipolar during their migration from the germinal layers to the cortical plate (CP) by forming a leading process and an axon that extends in the intermediate zone (IZ). Once they settle in the CP, neurons assume a highly polarized morphology with a single axon and multiple dendrites. The AMPK-related kinases SadA and SadB are intrinsic factors that are essential for axon formation during neuronal development downstream of Lkb1. The knockout of both genes encoding Sad kinases (Sada and Sadb) results not only in a loss of axons but also a decrease in the size of the cortical plate. The defect in axon formation has been linked to a function of Sad kinases in the regulation of microtubule binding proteins. However, the causes for the reduced size of the cortical plate in the Sada-/-;Sadb-/- knockout remain to be analyzed in detail. Here we show that neuronal cell death is increased and the number of neural progenitors is decreased in the Sada-/-;Sadb-/- CP. The reduced number of progenitors is a non-cell autonomous defect since they do not express Sad kinases. These defects are restricted to the neocortex while the hippocampus remains unaffected.</description><subject>Alzheimer's disease</subject><subject>Apoptosis</subject><subject>Axonogenesis</subject><subject>Axons</subject><subject>Biology and Life Sciences</subject><subject>Brain research</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cells (biology)</subject><subject>Defects</subject><subject>Dendrites</subject><subject>Feedback</subject><subject>Genotype & phenotype</subject><subject>Kinases</subject><subject>LKB1 protein</subject><subject>Mammals</subject><subject>Medicine and Health Sciences</subject><subject>Morphology</subject><subject>Neocortex</subject><subject>Neural stem cells</subject><subject>Neurons</subject><subject>Progenitor cells</subject><subject>Protein binding</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Subventricular 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Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dhumale, Pratibha</au><au>Menon, Sindhu</au><au>Chiang, Joanna</au><au>Püschel, Andreas W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The loss of the kinases SadA and SadB results in early neuronal apoptosis and a reduced number of progenitors</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2018-04-26</date><risdate>2018</risdate><volume>13</volume><issue>4</issue><spage>e0196698</spage><epage>e0196698</epage><pages>e0196698-e0196698</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The neurons that form the mammalian neocortex originate from progenitor cells in the ventricular (VZ) and subventricular zone (SVZ). Newborn neurons are multipolar but become bipolar during their migration from the germinal layers to the cortical plate (CP) by forming a leading process and an axon that extends in the intermediate zone (IZ). Once they settle in the CP, neurons assume a highly polarized morphology with a single axon and multiple dendrites. The AMPK-related kinases SadA and SadB are intrinsic factors that are essential for axon formation during neuronal development downstream of Lkb1. The knockout of both genes encoding Sad kinases (Sada and Sadb) results not only in a loss of axons but also a decrease in the size of the cortical plate. The defect in axon formation has been linked to a function of Sad kinases in the regulation of microtubule binding proteins. However, the causes for the reduced size of the cortical plate in the Sada-/-;Sadb-/- knockout remain to be analyzed in detail. Here we show that neuronal cell death is increased and the number of neural progenitors is decreased in the Sada-/-;Sadb-/- CP. The reduced number of progenitors is a non-cell autonomous defect since they do not express Sad kinases. These defects are restricted to the neocortex while the hippocampus remains unaffected.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29698519</pmid><doi>10.1371/journal.pone.0196698</doi><tpages>e0196698</tpages><orcidid>https://orcid.org/0000-0002-0861-8863</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer's disease Apoptosis Axonogenesis Axons Biology and Life Sciences Brain research Cell cycle Cell death Cells (biology) Defects Dendrites Feedback Genotype & phenotype Kinases LKB1 protein Mammals Medicine and Health Sciences Morphology Neocortex Neural stem cells Neurons Progenitor cells Protein binding Proteins Research and Analysis Methods Rodents Subventricular zone Ventricle |
| title | The loss of the kinases SadA and SadB results in early neuronal apoptosis and a reduced number of progenitors |
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