Abstract:
:Nucleokinesis has recently been suggested as a critical regulator of neuronal migration. Here we show that Disabled 1 (Dab1), which is required for neuronal positioning in mammals, regulates the nuclear position of postmitotic neurons in a phosphorylation-site dependent manner. Dab1 expression in the Drosophila visual system partially rescues nuclear position defects caused by a mutation in the Dynactin subunit Glued. Furthermore, we observed that a loss-of-function allele of amyloid precursor protein (APP)-like, a kinesin cargo receptor, enhanced the severity of a Dab1 overexpression phenotype characterized by misplaced nuclei in the adult retina. In mammalian neurons, overexpression of APP reduced the ability of Reelin to induce Dab1 tyrosine phosphorylation, suggesting an antagonistic relationship between APP family members and Dab1 function. This is the first evidence that signaling which regulates Dab1 tyrosine phosphorylation determines nuclear positioning through Dab1-mediated influences on microtubule motor proteins in a subset of neurons.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Pramatarova A,Ochalski PG,Lee CH,Howell BWdoi
10.1128/MCB.26.4.1510-1517.2006subject
Has Abstractpub_date
2006-02-01 00:00:00pages
1510-7issue
4eissn
0270-7306issn
1098-5549pii
26/4/1510journal_volume
26pub_type
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