Centrosomal microtubule nucleation regulates radial migration of projection neurons independently of polarization in the developing brain
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F44555601%3A13440%2F23%3A43897675" target="_blank" >RIV/44555601:13440/23:43897675 - isvavai.cz</a>
Výsledek na webu
<a href="https://www.sciencedirect.com/science/article/pii/S0896627323000703?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0896627323000703?via%3Dihub</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.neuron.2023.01.020" target="_blank" >10.1016/j.neuron.2023.01.020</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Centrosomal microtubule nucleation regulates radial migration of projection neurons independently of polarization in the developing brain
Popis výsledku v původním jazyce
Cortical projection neurons polarize and form an axon while migrating radially. Even though these dynamic processes are closely interwoven, they are regulated separately-the neurons terminate their migration when reaching their destination, the cortical plate, but continue to grow their axons. Here, we show that in rodents, the centrosome distinguishes these processes. Newly developed molecular tools modulating centrosomal microtubule nucleation combined with in vivo imaging uncovered that dysregulation of centro-somal microtubule nucleation abrogated radial migration without affecting axon formation. Tightly regu-lated centrosomal microtubule nucleation was required for periodic formation of the cytoplasmic dilation at the leading process, which is essential for radial migration. The microtubule nucleating factor g-tubulin decreased at neuronal centrosomes during the migratory phase. As distinct microtubule networks drive neuronal polarization and radial migration, this provides insight into how neuronal migratory defects occur without largely affecting axonal tracts in human developmental cortical dysgeneses, caused by mutations in g-tubulin.
Název v anglickém jazyce
Centrosomal microtubule nucleation regulates radial migration of projection neurons independently of polarization in the developing brain
Popis výsledku anglicky
Cortical projection neurons polarize and form an axon while migrating radially. Even though these dynamic processes are closely interwoven, they are regulated separately-the neurons terminate their migration when reaching their destination, the cortical plate, but continue to grow their axons. Here, we show that in rodents, the centrosome distinguishes these processes. Newly developed molecular tools modulating centrosomal microtubule nucleation combined with in vivo imaging uncovered that dysregulation of centro-somal microtubule nucleation abrogated radial migration without affecting axon formation. Tightly regu-lated centrosomal microtubule nucleation was required for periodic formation of the cytoplasmic dilation at the leading process, which is essential for radial migration. The microtubule nucleating factor g-tubulin decreased at neuronal centrosomes during the migratory phase. As distinct microtubule networks drive neuronal polarization and radial migration, this provides insight into how neuronal migratory defects occur without largely affecting axonal tracts in human developmental cortical dysgeneses, caused by mutations in g-tubulin.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2023
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Neuron
ISSN
0896-6273
e-ISSN
1097-4199
Svazek periodika
111
Číslo periodika v rámci svazku
8
Stát vydavatele periodika
NL - Nizozemsko
Počet stran výsledku
40
Strana od-do
"nestrankovano"
Kód UT WoS článku
000984091400001
EID výsledku v databázi Scopus
2-s2.0-85149736432