Centrosomal microtubule nucleation regulates radial migration of projection neurons independently of polarization in the developing brain
The result's identifiers
Result code in 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>
Result on the web
<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>
Alternative languages
Result language
angličtina
Original language name
Centrosomal microtubule nucleation regulates radial migration of projection neurons independently of polarization in the developing brain
Original language description
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.
Czech name
—
Czech description
—
Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
—
OECD FORD branch
10608 - Biochemistry and molecular biology
Result continuities
Project
—
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2023
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Neuron
ISSN
0896-6273
e-ISSN
1097-4199
Volume of the periodical
111
Issue of the periodical within the volume
8
Country of publishing house
NL - THE KINGDOM OF THE NETHERLANDS
Number of pages
40
Pages from-to
"nestrankovano"
UT code for WoS article
000984091400001
EID of the result in the Scopus database
2-s2.0-85149736432