Genetic Analysis of PLA2G6 in 22 Indian Families with Infantile Neuroaxonal Dystrophy, Atypical Late-Onset Neuroaxonal Dystrophy and Dystonia Parkinsonism Complex

被引:25
|
作者
Kapoor, Saketh [1 ]
Shah, Mohd Hussain [1 ]
Singh, Nivedita [1 ]
Rather, Mohammad Iqbal [1 ]
Bhat, Vishwanath [1 ]
Gopinath, Sindhura [2 ]
Bindu, Parayil Sankaran [3 ]
Taly, Arun B. [3 ]
Sinha, Sanjib [3 ]
Nagappa, Madhu [3 ]
Bharath, Rose Dawn [4 ]
Mahadevan, Anita [5 ]
Narayanappa, Gayathri [5 ]
Chickabasaviah, Yasha T. [5 ]
Kumar, Arun [1 ]
机构
[1] Indian Inst Sci, Dept Mol Reprod Dev & Genet, Bangalore 560012, Karnataka, India
[2] RV Coll Engn, Dept Biotechnol, Bangalore 560059, Karnataka, India
[3] Natl Inst Mental Hlth & Neurosci, Dept Neurol, Bangalore 560029, Karnataka, India
[4] Natl Inst Mental Hlth & Neurosci, Dept Neuroimaging & Intervent Radiol, Bangalore 560029, Karnataka, India
[5] Natl Inst Mental Hlth & Neurosci, Dept Neuropathol, Bangalore 560029, Karnataka, India
来源
PLOS ONE | 2016年 / 11卷 / 05期
关键词
PHOSPHOLIPASE A(2); PHENOTYPIC SPECTRUM; MUTATION; MODEL;
D O I
10.1371/journal.pone.0155605
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Mutations in PLA2G6 were identified in patients with a spectrum of neurodegenerative conditions, such as infantile neuroaxonal dystrophy (INAD), atypical late-onset neuroaxonal dystrophy (ANAD) and dystonia parkinsonism complex (DPC). However, there is no report on the genetic analysis of families with members affected with INAD, ANAD and DPC from India. Therefore, the main aim of this study was to perform genetic analysis of 22 Indian families with INAD, ANAD and DPC. DNA sequence analysis of the entire coding region of PLA2G6 identified 13 different mutations, including five novel ones (p.Leu224Pro, p.Asp283Asn, p.Arg329Cys, p.Leu491Phe, and p.Arg649His), in 12/22 (54.55%) families with INAD and ANAD. Interestingly, one patient with INAD was homozygous for two different mutations, p.Leu491Phe and p.Ala516Val, and thus harboured four mutant alleles. With these mutations, the total number of mutations in this gene reaches 129. The absence of mutations in 10/22 (45.45%) families suggests that the mutations could be in deep intronic or promoter regions of this gene or these families could have mutations in a yet to be identified gene. The present study increases the mutation landscape of PLA2G6. The present finding will be useful for genetic diagnosis, carrier detection and genetic counselling to families included in this study and other families with similar disease condition.
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页数:12
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