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To better understand gene variants that underlie disease predispositions related to Treg functions and to identify regulatory networks related to both Treg and Th cells, we undertook a systems genetics analysis of gene expression in these cell types using a genetic reference panel consisting of 31 members of the large BXD family of recombinant inbred strains [ 13, 14].
In the Genome of the Netherlands project, the differentiation criterion for setting up a genetic reference database is nationality.
A genetic reference population of B6 X D2 (BXD) recombinant inbred lines made by crossing these parental strains has been used extensively to explore differences in gene expression, neuropharmacology, and behavior, often using quantitative trait locus (QTL) mapping methods [11], [12].
In this paper, we further demonstrated that the epigenetic-genetic chromosome dosage approach can be applied to the prenatal diagnosis of trisomy 21 using a fetal-specific SNP allele as a genetic reference baseline in place of a chromosome Y marker derived from a male fetus.
Finding the genetic source of this variation and identifying the functional associates requires a genetic reference population that has been broadly characterized for brain and behavioural function.
Because the genetic variation in BXD mice is between line rather than between animal, the BXD panel is a genetic reference population (a retrievable resource).
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To probe the genetic architecture of a polygenic phenotype as complex as NPC proliferation requires a large genetic reference panel that can provide high resolution and power to identify genes with subtle but significant effects on NPC proliferation.
These RILs are a stable genetic reference panel that allows for high-powered and high-resolution quantitative trait loci (QTL) mapping in the D. melanogaster model system.
Therefore, in order to fully appreciate the complexity of this process, we explored a separate genetic reference panel called the BXDs.
Elucidating the mechanisms by which susceptibility traits relate to addiction can be achieved through continual aggregation of molecular, physiological, morphological and behavioral data in a mouse genetic reference population (Plomin et al. 1991).
Integration of rich phenotypic and genomic data over time and across a wide variety of fields will be vital to delivering on one of the key attributes of the CC, a common genetic reference platform for identifying causative variants and genetic networks determining traits in mammals.
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