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The Drosophila melanogaster homolog of UBE3A is not imprinted in neurons
被引:5
|作者:
Hope, Kevin A.
[1
,2
]
LeDoux, Mark S.
[1
,2
]
Reiter, Lawrence T.
[1
,2
,3
]
机构:
[1] Univ Tennessee, Ctr Hlth Sci, Dept Neurol, 855 Monroe Ave,Link 415, Memphis, TN 38163 USA
[2] Univ Tennessee, Ctr Hlth Sci, Dept Anat & Neurobiol, Memphis, TN 38163 USA
[3] Univ Tennessee, Ctr Hlth Sci, Pediat, Memphis, TN 38163 USA
来源:
基金:
美国国家卫生研究院;
关键词:
Climbing assay;
DGRP;
Drosophila melanogaster;
ERG;
imprinting;
synaptic transmission;
SNPs;
UBE3A;
PRADER-WILLI SYNDROMES;
ANGELMAN-SYNDROME;
UBIQUITIN LIGASE;
EXPRESSION;
UBE3A/E6-AP;
DISORDERS;
BRAIN;
GENE;
D O I:
10.1080/15592294.2016.1214783
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
of the In mammals, expression of UBE3A is epigenetically regulated in neurons and expression is restricted to the maternal copy of UBE3A. A recent report claimed that Drosophila melanogaster UBE3A homolog (Dube3a) is preferentially expressed from the maternal allele in fly brain, inferring an imprinting mechanism. However, complex epigenetic regulatory features of the mammalian imprinting center are not present in Drosophila, and allele specific expression of Dube3a has not been documented. We used behavioral and electrophysiological analysis Dube3a loss-of-function allele (Dube3a(15b)) to investigate Dube3a imprinting in fly neurons. We found that motor impairment (climbing ability) and a newly-characterized defect in synaptic transmission are independent of parental inheritance of the Dube3a(15b) allele. Furthermore, expression analysis of coding single nucleotide polymorphisms (SNPs) in Dube3a did not reveal allele specific expression differences among reciprocal crosses. These data indicate that Dube3a is neither imprinted nor preferentially expressed from the maternal allele in fly neurons.
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页码:637 / 642
页数:6
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