Dramatic mutation instability in HD mouse striatum: does polyglutamine load contribute to cell-specific vulnerability in Huntington's disease?

被引:156
作者
Kennedy, L [1 ]
Shelbourne, PF [1 ]
机构
[1] Univ Glasgow, Inst Biomed & Life Sci, Div Mol Genet, Glasgow G11 6NU, Lanark, Scotland
关键词
D O I
10.1093/hmg/9.17.2539
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
An unstable CAG triplet repeat expansion encoding a polyglutamine stretch within the ubiquitously expressed protein huntingtin is responsible for causing Huntington's disease (HD). By quantifying the repeat sizes of individual mutant alleles in tissues derived from an accurate genetic mouse model of HD we show that the mutation becomes very unstable in striatal tissue. The expansion-biased changes increase with age, such that some striatal cells from old HD mice contain mutations that have tripled in size. If this pattern of repeat instability is recapitulated in human striatal tissue, the concomitant increased polyglutamine load may contribute to the patterns of selective neuronal cell death in HD. Our findings also suggest that trinucleotide repeat instability can occur by mechanisms that are not replication-based.
引用
收藏
页码:2539 / 2544
页数:6
相关论文
共 32 条
[1]   THE RELATIONSHIP BETWEEN TRINUCLEOTIDE (CAG) REPEAT LENGTH AND CLINICAL-FEATURES OF HUNTINGTONS-DISEASE [J].
ANDREW, SE ;
GOLDBERG, YP ;
KREMER, B ;
TELENIUS, H ;
THEILMANN, J ;
ADAM, S ;
STARR, E ;
SQUITIERI, F ;
LIN, BY ;
KALCHMAN, MA ;
GRAHAM, RK ;
HAYDEN, MR .
NATURE GENETICS, 1993, 4 (04) :398-403
[2]   CAG EXPANSION AFFECTS THE EXPRESSION OF MUTANT HUNTINGTIN IN THE HUNTINGTONS-DISEASE BRAIN [J].
ARONIN, N ;
CHASE, K ;
YOUNG, C ;
SAPP, E ;
SCHWARZ, C ;
MATTA, N ;
KORNREICH, R ;
LANDWEHRMEYER, B ;
BIRD, E ;
BEAL, MF ;
VONSATTEL, JP ;
SMITH, T ;
CARRAWAY, R ;
BOYCE, FM ;
YOUNG, AB ;
PENNEY, JB ;
DIFIGLIA, M .
NEURON, 1995, 15 (05) :1193-1201
[3]  
Cardozo-Pelaez F, 1999, MOVEMENT DISORD, V14, P972, DOI 10.1002/1531-8257(199911)14:6<972::AID-MDS1010>3.0.CO
[4]  
2-0
[5]   SOMATIC EXPANSION OF THE (CAG)(N) REPEAT IN HUNTINGTON DISEASE BRAINS [J].
DEROOIJ, KE ;
GANS, PAMD ;
ROOS, RAC ;
VANOMMEN, GJB ;
DENDUNNEN, JT .
HUMAN GENETICS, 1995, 95 (03) :270-274
[6]   TRINUCLEOTIDE REPEAT LENGTH INSTABILITY AND AGE-OF-ONSET IN HUNTINGTONS-DISEASE [J].
DUYAO, M ;
AMBROSE, C ;
MYERS, R ;
NOVELLETTO, A ;
PERSICHETTI, F ;
FRONTALI, M ;
FOLSTEIN, S ;
ROSS, C ;
FRANZ, M ;
ABBOTT, M ;
GRAY, J ;
CONNEALLY, P ;
YOUNG, A ;
PENNEY, J ;
HOLLINGSWORTH, Z ;
SHOULSON, I ;
LAZZARINI, A ;
FALEK, A ;
KOROSHETZ, W ;
SAX, D ;
BIRD, E ;
VONSATTEL, J ;
BONILLA, E ;
ALVIR, J ;
CONDE, JB ;
CHA, JH ;
DURE, L ;
GOMEZ, F ;
RAMOS, M ;
SANCHEZRAMOS, J ;
SNODGRASS, S ;
DEYOUNG, M ;
WEXLER, N ;
MOSCOWITZ, C ;
PENCHASZADEH, G ;
MACFARLANE, H ;
ANDERSON, M ;
JENKINS, B ;
SRINIDHI, J ;
BARNES, G ;
GUSELLA, J ;
MACDONALD, M .
NATURE GENETICS, 1993, 4 (04) :387-392
[7]   Dramatic, expansion-biased, age-dependent, tissue specific somatic mosaicism in a transgenic mouse model of triplet repeat instability [J].
Fortune, MT ;
Vassilopoulos, C ;
Coolbaugh, MI ;
Siciliano, MJ ;
Monckton, DG .
HUMAN MOLECULAR GENETICS, 2000, 9 (03) :439-445
[8]   EVIDENCE FOR DEGENERATIVE AND REGENERATIVE CHANGES IN NEOSTRIATAL SPINY NEURONS IN HUNTINGTONS-DISEASE [J].
GRAVELAND, GA ;
WILLIAMS, RS ;
DIFIGLIA, M .
SCIENCE, 1985, 227 (4688) :770-773
[9]  
Harper P.S., 1996, Huntington's Disease, V2nd
[10]   Rapid aggregate formation of the huntingtin N-terminal fragment carrying an expanded polyglutamine tract [J].
Hazeki, N ;
Nakamura, K ;
Goto, J ;
Kanazawa, I .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 256 (02) :361-366