このエントリーをはてなブックマークに追加
ID 48960
FullText URL
Author
Okada, Yasukazu
Teramura, Kouhei
Abstract
Developmental processes of organisms are programed to proceed in a finely regulated manner and finish within a certain period of time depending on the ambient environmental conditions. Therefore, variation in the developmental period under controlled genetic and environmental conditions indicates innate instability of the developmental process. In this study, we aimed to determine whether a molecular machinery exists that regulates the canalization of the developmental period and, if so, to test whether the same mechanism also stabilizes a morphological trait. To search for regions that influence the instability of the developmental period, we conducted genome-wide deficiency mapping with 441 isogenic deficiency strains covering 65.5% of the Drosophila melanogaster genome. We found that 11 independent deficiencies significantly increased the instability of the developmental period and 5 of these also significantly increased the fluctuating asymmetry of wing shape although there was no significant correlation between the instabilities of developmental period and wing shape in general. These results suggest that canalization processes of the developmental period and morphological traits are at least partially independent. Our findings emphasize the potential importance of temporal variation in development as an indicator of developmental stability and canalization and provide a novel perspective for understanding the regulation of phenotypic variability.
Keywords
developmental period
developmental stability
Drosophila melanogaster
wing shape
Published Date
2011-08
Publication Title
Journal of Heredity
Volume
volume102
Issue
issue4
Publisher
Oxford University Press
Start Page
448
End Page
457
ISSN
0022-1503
Content Type
Journal Article
Project
Research Core for Interdisciplinary Sciences
Official Url
http://jhered.oxfordjournals.org/content/early/2011/04/27/jhered.esr026.short?rss=1
language
英語
Copyright Holders
© The American Genetic Association. 2011. All rights reserved.
File Version
author
Refereed
True
DOI
PubMed ID
Web of Science KeyUT