The Long Path from QTL to Gene

Norman R Drinkwater,Michael N Gould,H Leighton Grimes

doi:10.1371/journal.pgen.1002975

Norman R Drinkwater, Michael N Gould + Show 1 more

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https://doi.org/10.1371/journal.pgen.1002975

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Journal: PLoS Genetics	Publication Date: Sep 20, 2012
Citations: 52	License type: CC BY 4.0

Affiliation: University of Wisconsin–Madison

Abstract

The Long Path from QTL to Gene

Highlights

The construction in the 1990s of high density genetic maps of the mouse and rat based on simple sequence length polymorphisms led to an explosion of activity directed toward the identification of quantitative trait loci (QTLs) that control a broad array of normal and abnormal biology
Mapping QTLs to higher resolution requires the time and resources to produce congenic lines that carry a limited interval of the high risk donor strain’s genome on the genetic background of the other strain, followed by phenotypic analysis of recombinant lines derived from that congenic
The ‘‘gold standard’’ for proof that a particular candidate is the causative gene by transgenesis or allelic substitution by homologous recombination has been achieved in only a few cases, but analysis of gene knockout strains or demonstration of specific genetic or epigenetic alterations in the orthologue in human tumors has more often provided a weight of evidence in favor of a particular candidate

Summary

Introduction

The construction in the 1990s of high density genetic maps of the mouse and rat based on simple sequence length polymorphisms led to an explosion of activity directed toward the identification of quantitative trait loci (QTLs) that control a broad array of normal and abnormal biology. That complexity has prompted many investigators, including Hunter and colleagues (whose work is presented in this issue, [4]), to pursue the identification of cancer modifier genes, QTLs that alter cancer development in rodents.

Results

Conclusion