RGD Reference Report - Tissue-Specific Actions of the Ept1, Ept2, Ept6, and Ept9 Genetic Determinants of Responsiveness to Estrogens in the Female Rat. - Rat Genome Database

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Tissue-Specific Actions of the Ept1, Ept2, Ept6, and Ept9 Genetic Determinants of Responsiveness to Estrogens in the Female Rat.

Authors: Kurz, SG  Hansen, KK  McLaughlin, MT  Shivaswamy, V  Schaffer, BS  Gould, KA  McComb, RD  Meza, JL  Shull, JD 
Citation: Kurz SG, etal., Endocrinology. 2008 Apr 17;.
RGD ID: 2292503
Pubmed: PMID:18420736   (View Abstract at PubMed)
PMCID: PMC2488241   (View Article at PubMed Central)
DOI: DOI:10.1210/en.2008-0173   (Journal Full-text)

Ept1, Ept2, Ept6 and Ept9 are quantitative trait loci (QTL) mapped in crosses between the ACI and Copenhagen (COP) rat strains as genetic determinants of responsiveness of the pituitary gland to estrogens. We have developed four congenic rat strains, each of which carries, on the genetic background of the ACI rat strain, alleles from the COP rat strain that span one of these QTL. Relative to the female ACI rats, female ACI.COP-Ept1 rats exhibited reduced responsiveness to 17beta-estradiol (E2) in the pituitary gland, as evidenced by quantification of pituitary mass and circulating prolactin (PRL), and in the mammary gland, as evidenced by reduced susceptibility to E2-induced mammary cancer. The ACI.COP-Ept2 rat strain exhibited reduced responsiveness to E2 in the pituitary gland, but did not differ from the ACI strain in regard to susceptibility to E2-induced mammary cancer. Interestingly, female Ept2 congenic rats exhibited increased responsiveness to E2 in the thymus, as evidenced by enhanced thymic atrophy. The ACI.COP-Ept6 rat strain exhibited increased responsiveness to E2 in the pituitary gland, which was associated with a qualitative phenotype suggestive of enhanced pituitary vascularization. The ACI.COP-Ept9 rat strain exhibited reduced responsiveness to E2 in the anterior pituitary gland, relative to the ACI rat strain. Neither Ept6 nor Ept9 impacted responsiveness to E2 in the mammary gland or thymus. These data indicate that each of these Ept genetic determinants of estrogen action is unique in regard to the tissues in which it exerts its effects and/or the direction of its effect on estrogen responsiveness.



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Objects Annotated

QTLs
Emca10  (Estrogen-induced mammary cancer QTL 10)
Ept15  (Estrogen-induced pituitary tumorigenesis QTL 15)
Ept16  (Estrogen-induced pituitary tumorigenesis QTL 16)
Ept17  (Estrogen-induced pituitary tumorigenesis QTL 17)
Ept18  (Estrogen-induced pituitary tumorigenesis QTL 18)
Esta4  (Estrogen-induced thymic atrophy QTL 4)

Objects referenced in this article
QTL Ept1 Estrogen-induced pituitary tumorigenesis QTL 1 Rattus norvegicus
QTL Ept2 Estrogen-induced pituitary tumorigenesis QTL 2 Rattus norvegicus
QTL Ept6 Estrogen-induced pituitary tumorigenesis QTL 6 Rattus norvegicus
QTL Ept9 Estrogen-induced pituitary tumorigenesis QTL 9 Rattus norvegicus

Additional Information