RGD Reference Report - Genetic control of estrogen action in the rat: mapping of QTLs that impact pituitary lactotroph hyperplasia in a BN x ACI intercross. - Rat Genome Database

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Genetic control of estrogen action in the rat: mapping of QTLs that impact pituitary lactotroph hyperplasia in a BN x ACI intercross.

Authors: Shull, JD  Lachel, CM  Murrin, CR  Pennington, KL  Schaffer, BS  Strecker, TE  Gould, KA 
Citation: Shull JD, etal., Mamm Genome. 2007 Sep 18;.
RGD ID: 1642526
Pubmed: PMID:17876666   (View Abstract at PubMed)
DOI: DOI:10.1007/s00335-007-9052-2   (Journal Full-text)

Estrogens are important regulators of growth and development and contribute to the etiology of several types of cancer. Different inbred rat strains exhibit marked, cell-type-specific differences in responsiveness to estrogens as well as differences in susceptibility to estrogen-induced tumorigenesis. Regulation of pituitary lactotroph homeostasis is one estrogen-regulated response that differs dramatically between different inbred rat strains. In this article we demonstrate that the growth response of the anterior pituitary gland of female ACI rats to 17beta-estradiol (E2) markedly exceeds that of identically treated female Brown Norway (BN) rats. We further demonstrate that pituitary mass, a surrogate indicator of absolute lactotroph number, behaves as a quantitative trait in E2-treated F(2) progeny generated in a genetic cross originating with BN females and ACI males. Composite interval mapping analyses of the (BNxACI)F(2) population revealed quantitative trait loci (QTLs) that exert significant effects on E2-induced pituitary growth on rat chromosome 4 (RNO4) (Ept5) and RNO7 (Ept7). Continuous treatment with E2 rapidly induces mammary cancer in female ACI rats but not BN rats, and QTLs that impact susceptibility to E2-induced mammary cancer in the (BNxACI)F(2) population described here have been mapped to RNO3 (Emca5), RNO4 (Emca6), RNO5 (Emca8), RNO6 (Emca7), and RNO7 (Emca4). Ept5 and Emca6 map to distinct regions of RNO4. However, Ept7 and Emca4 map to the same region of RNO7. No correlation between pituitary mass and mammary cancer number at necropsy was observed within the (BNxACI)F(2) population. This observation, together with the QTL mapping data, indicate that with the exception of the Ept7/Emca4 locus on RNO7, the genetic determinants of E2-induced pituitary growth differ from the genetic determinants of susceptibility to E2-induced mammary cancer.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Pituitary Neoplasms  IDA 1642526; 1642526 RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
decreased pituitary gland weight inducedIAGP17 beta-estradiol1642526compared to treated ACI/SegHsdRGD 
decreased pituitary gland weight  IAGP 1642526compared to ACI/SegHsdRGD 
increased pituitary gland weight inducedIAGP17 beta-estradiol1642526compared with ACI/SedHsd and treated BN/SsNHsdRGD 
increased pituitary gland weight inducedIAGP17 beta-estradiol1642526compared to BN/SsNHsdRGD 
pituitary gland hyperplasia  IDA 1642526; 1642526 RGD 

Related Phenotype Data for this Reference

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Objects Annotated

QTLs
Ept5  (Estrogen-induced pituitary tumorigenesis QTL 5)
Ept7  (Estrogen-induced pituitary tumorigenesis QTL 7)

Strains
ACI/SegHsd  (NA)
BN/SsNHsd  (NA)


Additional Information