Skip Navigation



Journal of Heredity Advance Access published online on December 23, 2004

Journal of Heredity, doi:10.1093/jhered/esi017
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
96/2/85    most recent
esi017v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by DeWoody, Y. D.
Right arrow Articles by DeWoody, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by DeWoody, Y. D.
Right arrow Articles by DeWoody, J. A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2005 The American Genetic Association
Received June 1, 2004
Accepted August 15, 2004

Article

On the Estimation of Genome-wide Heterozygosity Using Molecular Markers

Y. D. DeWoody 1 and J. A. DeWoody 1*

1 From the Department of Forestry and Natural Resources, Purdue University, West Lafayette, IN 47907-1159

* To whom correspondence should be addressed.
J. A. DeWoody, E-mail: dewoody{at}purdue.edu


   Abstract

Coltman and Slate (2003) recently performed a meta-analysis on studies that investigated the association between genetic variation at microsatellite loci and phenotypic trait variation. One factor not explicitly addressed in their meta-analysis is the actual estimation of genome-wide heterozygosity via molecular markers. Many authors still associate marker-estimated heterozygosity with genome-wide heterozygosity, despite allozyme-based evidence that such correlations are usually very weak or nonexistent. Here, we show that genome-wide heterozygosity is poorly estimated not only by allozymes but also by microsatellite loci and by single-nucleotide polymorphisms (SNPs). Thus, associations between fitness (or other phenotypes) and heterozygosity should be established firmly on causative factors and not on simple correlations.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J HeredHome page
J. A. Ivy, A. Miller, R. C. Lacy, and J. A. DeWoody
Methods and Prospects for Using Molecular Data in Captive Breeding Programs: An Empirical Example Using Parma Wallabies (Macropus parma)
J. Hered., July 1, 2009; 100(4): 441 - 454.
[Abstract] [Full Text] [PDF]


Home page
Proc R Soc BHome page
A. K. Townsend, A. B. Clark, K. J. McGowan, E. L. Buckles, A. D. Miller, and I. J. Lovette
Disease-mediated inbreeding depression in a large, open population of cooperative crows
Proc R Soc B, June 7, 2009; 276(1664): 2057 - 2064.
[Abstract] [Full Text] [PDF]


Home page
J HeredHome page
J. M. Aparicio, J. Ortego, and P. J. Cordero
Can a Simple Algebraic Analysis Predict Markers-Genome Heterozygosity Correlations?
J. Hered., January 1, 2007; 98(1): 93 - 96.
[Abstract] [Full Text] [PDF]


Home page
Behav EcolHome page
P. M. Waser and J. A. De Woody
Multiple paternity in a philopatric rodent: the interaction of competition and choice
Behav. Ecol., November 1, 2006; 17(6): 971 - 978.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.