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Open Access Research article

Genome-wide deficiency screen for the genomic regions responsible for heat resistance in Drosophila melanogaster

Kazuo H Takahashi1*, Yasukazu Okada2 and Kouhei Teramura2

Author affiliations

1 Research Core for Interdisciplinary Sciences, Okayama University, 3-1-1, Tsushima-naka, Kita-ku, Okayama 700-8530, Japan

2 Graduate School of Environmental Science, Okayama University, 1-1-1, Tsushima-naka, Kita-ku, Okayama 700-8530, Japan

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Citation and License

BMC Genetics 2011, 12:57  doi:10.1186/1471-2156-12-57

Published: 22 June 2011



Temperature adaptation is one of the most important determinants of distribution and population size of organisms in nature. Recently, quantitative trait loci (QTL) mapping and gene expression profiling approaches have been used for detecting candidate genes for heat resistance. However, the resolution of QTL mapping is not high enough to examine the individual effects of various genes in each QTL. Heat stress-responsive genes, characterized by gene expression profiling studies, are not necessarily responsible for heat resistance. Some of these genes may be regulated in association with the heat stress response of other genes.


To evaluate which heat-responsive genes are potential candidates for heat resistance with higher resolution than previous QTL mapping studies, we performed genome-wide deficiency screen for QTL for heat resistance. We screened 439 isogenic deficiency strains from the DrosDel project, covering 65.6% of the Drosophila melanogaster genome in order to map QTL for thermal resistance. As a result, we found 19 QTL for heat resistance, including 3 novel QTL outside the QTL found in previous studies.


The QTL found in this study encompassed 19 heat-responsive genes found in the previous gene expression profiling studies, suggesting that they were strong candidates for heat resistance. This result provides new insights into the genetic architecture of heat resistance. It also emphasizes the advantages of genome-wide deficiency screen using isogenic deficiency libraries.