ELP3 localises to mitochondria and actin-rich domains at edges of HeLa cells

被引:12
作者
Barton, Deborah [1 ]
Braet, Filip [2 ]
Marc, Jan [1 ]
Overall, Robyn [1 ]
Gardiner, John [1 ]
机构
[1] Univ Sydney, Sch Biol Sci, Camperdown, NSW 2006, Australia
[2] Univ Sydney, Australian Key Ctr Microscopy & Microanal, Camperdown, NSW 2006, Australia
基金
澳大利亚研究理事会;
关键词
Familial dysautonomia; Motor neuron disease; Amyotrophic lateral sclerosis; ELONGATOR; ELP3; Actin; Mitochondria; ELONGATOR COMPLEX; FAMILIAL DYSAUTONOMIA; INTERACTION NETWORK; TRANSCRIPTION; PROTEIN; GENE; IMPAIRMENT; EXOCYTOSIS; MIGRATION;
D O I
10.1016/j.neulet.2009.03.006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
motor neuron disease is associated with mutations in the ELP3 protein. Familial dysautonomia is a hereditary disease of the autonomous nervous system that occurs due to a mutation in the I kappa B kinase complex-associated protein (IKAP). Both ELP3 and IKAP are components of the ELONGATOR histone acetylase complex. This complex has six subunits ELP1 (IKAP)-ELP6. ELP3 is the acetylase component of the complex and is known to play a key role in histone acetylation. However, ELONGATOR components including IKAP also localise to cytoplasmic compartments, including actin-rich membrane ruffles. Therefore it is likely that the ELP3 acetylase may also acetylate cytoplasmic proteins. Here, we show using immunofluorescence with two different antibodies against ELP3 that it localises to mitochondria in HeLa cells as well as actin-like filaments and actin-rich sites at the edges of spreading cells. This suggests that ELP3, and possibly the ELONGATOR complex may play a role in mitochondrial function, as well as in actin organisation and cell motility. Crown Copyright (C) 2009 Published by Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:60 / 64
页数:5
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