and Boys Tuwn National Institute, Omaha, N e b r a s k a 68131 (P.R.F.) The nature of the problems posed for the l l p segment of the fourth Genetic Analysis Workshop w e r e discussed in some detail i n the summary paper, as w e r e the characteristics of the two
Multipoint linkage analysis of spinocerebellar ataxia and markers on chromosome 6
β Scribed by Dr. J. L. Haines; J. A. Trofatter; D. C. Rao
- Publisher
- John Wiley and Sons
- Year
- 1986
- Tongue
- English
- Weight
- 330 KB
- Volume
- 3
- Category
- Article
- ISSN
- 0741-0395
No coin nor oath required. For personal study only.
β¦ Synopsis
Heterogeneity among the spinocerebellar ataxias (SCA) has been shown on clinical, biochemical, and genetic criteria. Among the autosomal dominant SCAs, several kindreds have shown loose linkage to the HLA loci on chromosome 6, while linkage in other kindreds has been rejected. The advent of multipoint linkage analysis allows the use of several marker loci simultaneously, thus increasing the amount of usable information. We have reanalyzed linkage data from a large kindred with SCA and provide evidence for a telomeric location of the SCA gene in this family. Knowledge of the relative gene location will ease the identification of the SCA gene by reducing the size of the chromosomal regions that must be examined.
π SIMILAR VOLUMES
## Abstract Variance component models form a powerful and flexible tool for multipoint linkage analysis of quantitative traits. Estimates of genetic similarity are needed for the variance component model to detect linkage and to locate genes, and two methods are commonly used to calculate multipoin
## Abstract Multipoint linkage methods are powerful tools that are often employed as the first means to discover alleles affecting liability to diseases. With the advent of dense marker maps, linkage disequilibrium (LD) between markers is inevitable and it comes at the cost of bias and an increased
Chdteau de Longchamp, C a r r e f o u r de Longchamp , Bois de Boulogne, 750 16 P a r i s , France.
In the first part of our study we tested linkage with chromosome 18 markers in a sample of bipolar I sib pairs. We did not obtain evidence for linkage but showed that we could not exclude the presence of a disease locus (having even a nonnegligible effect). The limitation of the sib-pair sample size