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1.
Angiogenesis and capillary maturation phenotypes associated with the Edpm3 locus on rat chromosome 3
The quantitative trait locus (QTL) Edpm3 is one of a group of additively acting QTL \responsible for the difference in estrogen-induced pituitary tumor growth between
the tumor-susceptible F344 and tumor-resistant BN rat strains. The F344.BN-Edpm3BN rat strain was produced by moving the segment of rat Chr 3 between D3Mgh7 and D3Mgh13, which contains the Edpm3 QTL, from the BN strain into the F344 genetic background. In a previous study, we used this congenic line to find that the
BN allele of the Edpm3 QTL reduces tissue mass and S-phase fraction in the estrogen-induced rat pituitary tumor. We now report on the use of this
congenic line to investigate the linkage of Edpm3 to tumor angiogenesis. Contrary to expectation, the F344.BN-Edpm3BN strain has significantly greater angiogenic activity than does F344 in both treated and untreated rats. Microvessel count
(MVC), perivascular space, and number of nonattached pericytes/pericapillary fibroblasts are all elevated in the pituitary
by chronic estrogen treatment and their values are significantly greater in F344.BN-Edpm3BN than F344. Thus, although there is greater angiogenic activity in the pituitary of estrogen-treated F344.BN-Edpm3BN rats, there is a deficiency in capillary maturation compared with F344. 相似文献
2.
Douglas L. Wendell Shannon B. Daun Matthew B. Stratton Jack Gorski 《Mammalian genome》2000,11(10):855-861
Estrogen treatment to rats of the Fischer 344 (F344) strain induces growth of pituitary tumors that exhibit accelerated cell
proliferation, breakdown of basement membrane, and formation of hemorrhagic lakes. Estrogen-dependent pituitary growth is
due to variation in a group of quantitative trait loci (QTL), called Edpm for estrogen-dependent pituitary mass, that we previously identified in an F2 intercross of F344 and the tumor-resistant Brown Norway strain. We previously identified 5 QTL, and microsatellite markers
developed since our earlier work have allowed us to scan new chromosomal regions, resulting in two new QTL for estrogen-dependent
pituitary mass: Edpm9-2 and a possible QTL on the X Chromosome (Chr). Here we report evidence that these QTL differ from each other in how they affect
growth. To examine the effect of the Edpm QTL on biochemical components of tumor growth, we tested their effects in 138 progeny of a backcross to the F344 strain which
were given a 10-week chronic estrogen treatment. Hemoglobin/DNA ratio (a measure of blood volume relative to cell number)
and total pituitary DNA (a measure of cell number) correlated only weakly, and very large pituitaries were observed which
had a low hemoglobin/DNA ratio resembling a normal gland. Through QTL mapping, we found that Edpm2-1, Edpm3, Edpm5, and Edpm9-2 all had significant effects on pituitary mass, but Edpm2-1 and Edpm9-2 primarily affected DNA content, Edpm5 primarily affected hemoglobin/DNA ratio, and Edpm3 affected all traits equally.
Received: 16 March 2000 / Accepted: 17 May 2000 相似文献
3.
Cracchiolo D Swick JW McKiernan L Sloan E Raina S Sloan C Wendell DL 《Experimental biology and medicine (Maywood, N.J.)》2002,227(7):492-499
Long-term (10-week) treatment of Fischer 344 (F344) rats with the synthetic estrogen diethylstilbestrol (DES) increases the level of vascular endothelial growth factor (VEGF) in the pituitary. This is concurrent with the development of a large tumor of the pituitary of F344 rats. A role for VEGF in estrogen-dependent pituitary tumor growth is also supported by the fact that pituitary VEGF level is not increased by estrogen treatment in rats of the tumor-resistant Brown Norway (BN) strain. However, VEGF is not increased by estrogen treatment in an F(1) hybrid of F344 and BN, even though F(1) hybrid rats do form pituitary tumors in response to estrogen. Quantitative trait locus (QLT) mapping reveals that control of estrogen-dependent VEGF expression is linked to the Edpm5 QTL, which was previously identified as a QTL for estrogen-dependent pituitary tumor growth. In contrast, the QTL Edpm2-1 and Edpm9-2, which have been shown to each have a significant effect on estrogen-dependent pituitary mass of a magnitude similar to Edpm5, do not have any effect on VEGF level. Taken together, our results support the association of VEGF expression with growth of the estrogen-induced rat pituitary tumor, as has been reported by others, but they also indicate that there is significant pathways of growth regulation that are independent of high-level VEGF expression. 相似文献
4.
Genetic dissection of ``OLETF', a rat model for non-insulin-dependent diabetes mellitus 总被引:3,自引:0,他引:3
Naohide Kanemoto Haretsugu Hishigaki Ayako Miyakita Keiko Oga Shiro Okuno Atsushi Tsuji Toshihisa Takagi Ei-ichi Takahashi Yusuke Nakamura Takeshi K. Watanabe 《Mammalian genome》1998,9(6):419-425
To elucidate the genetic factors underlying non-insulin-dependent diabetes mellitus (NIDDM), we performed genome-wide quantitative
trait locus (QTL) analysis, using the Otsuka Long-Evans Tokushima Fatty (OLETF) rat. The OLETF rat is an excellent animal
model of NIDDM because the features of the disease closely resemble human NIDDM. Genetic dissection with two kinds of F2 intercross
progeny, from matings between the OLETF rat and non-diabetic control rats F344 or BN, allowed us to identify on Chromosome
(Chr) 1 a major QTL associated with features of NIDDM that was common to both crosses. We also mapped two additional significant
loci, on Chrs 7 and 14, in the (OLETF × F344)F2 cross alone, and designated these three loci as Diabetes mellitus, OLETF type Dmo 1, Dmo2 and Dmo3 respectively. With regard to suggestive QTLs, we found loci on Chrs 10, 11, and 16 that were common to both crosses, as well
as loci on Chrs 5 and 12 in the (OLETF × F344)F2 cross and on Chrs 4 and 13 in the (OLETF × BN)F2 cross. Our results showed that NIDDM in the OLETF rat is polygenic and demonstrated that different genetic backgrounds could
affect ``fitness' for QTLs and produce different phenotypic effects from the same locus.
Received: 9 October 1997 / Accepted: 29 January 1998 相似文献
5.
Ogino T Moralejo DH Zhu M Toide K Wei S Wei K Yamada T Mizuno A Matsumoto K Shima K 《Genetical research》1999,73(1):29-36
The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for obese-type non-insulin-dependent diabetes mellitus (NIDDM) in humans. The OLETF rat exhibits sustained hyperglycaemia after partial pancreatectomy, while the normal control rat does not. This difference is thought to be genetically determined and to be caused by impairment of beta-cell regrowth, a possible event involved in the pathogenesis of NIDDM. Our investigation was designed to identify quantitative trait loci (QTL) responsible for post-pancreatectomy hyperglycaemia by performing a genome-wide scan in an F2 intercross obtained by mating the OLETF and Fischer-344 (F344) rats. We have identified three possible QTL on rat chromosomes (Chrs) 3, 14 and 19 that account for a total of approximately 75% of the genetic variance in the F2. For the QTL on Chr 14, the OLETF allele corresponds with increased glucose levels, as expected. Surprisingly, for the QTL on Chr 19, the F344 allele corresponds with increased glucose levels. The Chr 3 QTL exhibits heterosis, heterozygotes showing significantly higher glucose levels than OLETF or F344 homozygotes. We also found evidence for interaction (epistasis) between the QTL on Chrs 14 and 19. 相似文献
6.
T. Agui T. Miyamoto C.-G. Jung T. Tsumagari K. Masuda T. Manabe 《Mammalian genome》2000,11(10):862-865
The LEC rat has been reported to exhibit X-ray hypersensitivity and deficiency in DNA double-strand break (DSB) repair. The
present study was performed to map the locus responsible for this phenotype, the xhs (X-ray hypersensitivity), as the first step in identifying the responsible gene. Analysis of the progeny of (BN × LEC)F1× LEC backcrosses indicated that the X-ray hypersensitive phenotype was controlled by multiple genetic loci in contrast to
the results reported previously. Quantitative trait loci (QTL) linkage analysis revealed two responsible loci located on Chromosomes
(Chr) 4 and 1. QTL on Chr 4 exhibited very strong linkage to the X-ray hypersensitive phenotype, while QTL on Chr 1 showed
weak linkage. The Rad52 locus, mutation of which results in hypersensitivity to ionizing radiation and impairment of DNA DSB repair in yeast, was
reported to be located on the synteneic regions of mouse Chr 6 and human Chr 12. However, mapping of the rat Rad52 locus indicated that it was located 23 cM distal to the QTL on Chr 4. Furthermore, none of the radio-sensitivity-related
loci mapped previously in the rat chromosome were identical to the QTL on Chrs 4 and 1 in the LEC rat. Thus, it seems that
X-ray hypersensitivity in the LEC rat is caused by mutation(s) in as-yet-undefined genes.
Received: 14 February 2000 / Accepted: 17 May 2000 相似文献
7.
Elaine F. Remmers Ellen A. Goldmuntz Joseph M. Cash Hongbin Zha Leslie J. Crofford Barbara Misiewicz-Poltorak Peter Mathern Ronald L. Wilder 《Mammalian genome》1993,4(2):90-94
Seven polymorphic markers identified by polymerase chain reaction (PCR) amplification, including markers for six genes—DRD1L (dopamine receptor, D1-like-2), GLUKA (glucokinase), PF4 (platelet factor 4), ALB (albumin), AFP (-fetoprotein), and BSP (bone sialoprotein)—and one anonymous locus (D14N52), were mapped to a single 67-cM linkage group with F2 intercross progeny of F344/N and LEW/N inbred rat strains. Two of these markers, ALB and AFP, have previously been assigned to rat Chromosome (Chr) 14, allowing assignment of this entire linkage group. Five of the markers—DRD1L, PF4, ALB, AFP, and PBSP—have been physically mapped to a large region of human Chr 4 encompassing the p arm and the q arm to band q28. Homologs of two of the markers, ALB and AFP, have been mapped to Chr 5 in the mouse. Comparison of human Chr 4 with the homologous regions on Chr 14 of the rat and Chr 5 of the mouse indicated that linkage conservation with human Chr 4 extends over a greater region in the rat than in the mouse. The markers described here were found to be highly polymorphic in twelve inbred strains (F344/N, LEW/N, ACI/N, BUF/N, BN/SsN, LOU/MN, MNR/N, MR/N, SHR/N, WBB1/N, WBB2/N, and WKY/N). These polymorphic markers should be useful in genetic linkage studies of important phenotypes in rats. 相似文献
8.
James D. Shull Cynthia M. Lachel Clare R. Murrin Karen L. Pennington Beverly S. Schaffer Tracy E. Strecker Karen A. Gould 《Mammalian genome》2007,18(9):657-669
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 17β-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 F2 progeny generated in a genetic cross originating with BN females and ACI males. Composite interval mapping analyses of the
(BN×ACI)F2 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 (BN×ACI)F2 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 (BN×ACI)F2 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. 相似文献
9.
Lindy S. Klaff George Koike Jianjie Jiang Yanling Wang Sabine Bieg Anna Pettersson Eric Lander Howard Jacob Åke Lernmark 《Mammalian genome》1999,10(9):883-887
The genetic etiology of Type 1 (insulin-dependent) diabetes mellitus is complicated by the apparent presence of several diabetes
susceptibility genetic regions. Type 1 diabetes in the inbred BioBreeding (BB) rat closely resembles the human disorder and
was previously shown to involve two genes: the lymphopenia (lyp) region on Chromosome (Chr) 4 and RT1
u
in the major histocompatibility complex (MHC) on Chr 20. In addition, a segregation analysis of an F2 intercross between the diabetes-prone congenic BB DR
lyp/lyp,u/u
and F344+/+,
lv/lv
rats indicated that at least one more genetic factor was responsible for Type 1 diabetes. In this study, we generated F2N2 progeny in a cross between non-diabetic F2(DR
lyp/lyp,u/u
× F344)
lyp/lyp,u/u
and diabetic DR
lyp/lyp,u/u
rats. In a subsequent total genome scan, a third factor was mapped to the 21.3-cM region on Chr 2 between D2Mit14 and D2Mit15 (peak LOD score 4.7 with 67% penetrance). Interestingly, the homozygosity of the BB allele (b/b) for the Chr 2 region was significantly associated with a greater weight reduction after fasting than the homozygosity of
the F344 allele (f/f, p < 0.008). In conclusion, the development of Type 1 diabetes in the congenic DR
lyp/lyp
rat is controlled by at least three genes: lymphopenia, MHC, and a third factor that may play a role in metabolism and body
weight regulation.
Received: December 1998 / Accepted: 10 May 1999 相似文献
10.
Jieping Huang Ruihua Dang Daisuke Torigoe Chuzhao Lei Xianyong Lan Hong Chen Nobuya Sasaki Jinxi Wang Takashi Agui 《PloS one》2015,10(3)
Hirschsprung’s disease (HSCR) is a congenital disease in neonates characterized by the absence of the enteric ganglia in a variable length of the distal colon. This disease results from multiple genetic interactions that modulate the ability of enteric neural crest cells to populate developing gut. We previously reported that three rat strains with different backgrounds (susceptible AGH-Ednrbsl/sl, resistant F344-Ednrbsl/sl, and LEH-Ednrbsl/sl) but the same null mutation of Ednrb show varying severity degrees of aganglionosis. This finding suggests that strain-specific genetic factors affect the severity of HSCR. Consistent with this finding, a quantitative trait locus (QTL) for the severity of HSCR on chromosome (Chr) 2 was identified using an F2 intercross between AGH and F344 strains. In the present study, we performed QTL analysis using an F2 intercross between the susceptible AGH and resistant LEH strains to identify the modifier/resistant loci for HSCR in Ednrb-deficient rats. A significant locus affecting the severity of HSCR was also detected within the Chr 2 region. These findings strongly suggest that a modifier gene of aganglionosis exists on Chr 2. In addition, two potentially causative SNPs (or mutations) were detected upstream of a known HSCR susceptibility gene, Gdnf. These SNPs were possibly responsible for the varied length of gut affected by aganglionosis. 相似文献
11.
Ellen A. Goldmuntz Elaine F. Remmers Hongbin Zha Peter Mathern Ying Du Leslie J. Crofford Ronald L. Wilder 《Mammalian genome》1993,4(11):670-675
Seven polymorphic markers comprising a single linkage group were assigned to rat Chromosome (Chr) 5 by linkage analysis of the progeny of an F2 intercross of Fischer (F344/N) and Lewis (LEW/N) inbred rats. Three genes, -L-fucosidase 1 (FUCA1), mitochondrial superoxide dismutase (SOD2), and glucose transporter (GLUT1), were mapped by restriction fragment length polymorphism (RFLP) analysis. Two genes, glucose transporter (GTG3) and elastase II (ELAII), one pseudogene for tubulin (TUBAPS), and one sequence related to the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase gene (PFKFBP1-related sequence) were mapped by simple sequence repeat (SSR) polymorphism analysis. The loci are in the following order: SOD2, GTG3/GLUT1, FUCA1, ELAII/PFKFBP1-related sequence, and TUBAPS. This linkage group covered 68.3 cM of rat Chr 5. The SSR markers were highly polymorphic in 13 inbred rat strains (SHR/N, WKY/N, MNR/N, MR/N, LOU/MN, BN/SsN, BUF/N, WBB1/N, WBB2/N, ACI/N, LER/N, F344/N, and LEW/N). These markers, located on rat Chr 5, will be useful in genetic studies of inbred rats. 相似文献
12.
Quantitative trait loci (QTLs) affecting body weight were investigated in the backcross population derived from nondiabetic
BB/OK and spontaneously hypertensive rat (SHR) strains. The F1 hybrids were backcrossed onto SHR rats, and QTL analysis was performed separately with the resulting backcross populations
for each sex on Chromosomes (Chrs) 1, 3, 4, 10, 13, and 18. The body weight was determined at the age of 14 weeks, and the
statistical analysis was performed with MAPMAKER/QTL 1.1b computer program. According to the stringent threshold for a lod
score of 3.0, markers on Chr 1 were found to be linked with body weight. The QTL with a peak lod score (5.1) on Chr 1 for
a male population was located within markers Igf2 and D1Mgh12. In contrast, in the female population the body weight affecting QTL (lod = 5.7) on Chr 1 was located between the D1Mit3 and Lsn markers. The existence of QTLs on Chr 1 affecting body weight in the male population was confirmed by congenic BB.Sa rats,
carrying chromosomal region of SHR (Sa-Igf2) on the genetic background of BB rat.
Received: 14 July 1997 / Accepted: 22 December 1997 相似文献
13.
Norihiro Kato Gina Hyne Marie-Therese Bihoreau Dominique Gauguier G. Mark Lathrop John P. Rapp 《Mammalian genome》1999,10(3):259-265
The Dahl salt-sensitive rat is one of the principal animal models of hereditary hypertension. Genome-wide searches were undertaken
to detect quantitative trait loci (QTLs) that influence blood pressure, cardiac mass, and body weight in four F2 populations derived from Dahl salt-sensitive rats and different inbred normotensive control strains of rat. We detected three
QTLs associated with one or more of the phenotypes, using a stringent statistical criterion for linkage (p < 0.00003). These included a novel QTL linked to blood pressure on rat Chromosome (Chr) 12, and another QTL on rat Chr 3
linked to body weight. A QTL on rat Chr 10 for which linkage to blood pressure has been described in other crosses was found
to be a principal determinant of blood pressure and cardiac mass in some but not all of the crosses examined here. Three other
regions showed evidence of linkage to these phenotypes with a less stringent statistical criterion of linkage at QTLs previously
reported in other studies. As part of our study, microsatellite markers have been developed for three candidate genes for
investigation in hypertension, and the genes have been localized by linkage mapping. These are: the rat Gs alpha subunit (Gnas) gene, the alpha-1B adrenergic receptor (Adra1b), and the Na+, K+-ATPase beta2 subunit (Atp1b2) gene.
Received: 29 June 1998 / Accepted: 30 October 1998 相似文献
14.
Kenkichi Sugiura Takeshi Miyake Yukio Taniguchi Takahisa Yamada Daniel H. Moralejo Suwen Wei Kaichun Wei Yoshiyuki Sasaki Kozo Matsumoto 《Mammalian genome》1999,10(12):1126-1131
The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for obese-type, non-insulin-dependent diabetes mellitus
(NIDDM) in humans. We have previously identified 11 quantitative trait loci (QTLs) responsible for NIDDM susceptibility on
Chromosomes (Chrs) 1, 5, 7, 8, 9, 11, 12, 14, and 16 (Nidd1–11/of for Non-insulin-dependent diabetes1–11/oletf) by using the interval mapping method in 160 F2 progenies obtained by mating the OLETF and the Fischer-344 (F344) rats. MQM-mapping, which was applied for QTL analysis based
on multiple-QTL models, is reported to be more powerful than interval mapping, because in the process of mapping one QTL the
genetic background, which contains the other QTLs, is controlled. Application of MQM-mapping in the F2 intercrosses has led to a revelation of three novel QTLs on rat Chrs 5 (Nidd12/of), 7 (Nidd13/of), and 17 (Nidd14/of), in addition to Nidd1–11/of loci. The three QTLs, together with the Nidd1–11/of, account for a total of ∼70% and ∼85% of the genetic variance of the fasting and postprandial glucose levels, respectively,
in the F2. While the OLETF allele corresponds with increased glucose levels as expected for Nidd12 and 14/of, the Nidd13/of exhibits heterosis: heterozygotes showing significantly higher glucose levels than OLETF or F344 homozygotes. There is epistatic
interaction between Nidd2 and 14/of. Additionally, our results indicated that the novel QTLs could show no linkage with body weight, but Nidd12/of has an interaction with body weight.
Received: 23 February 1999 / Accepted: 3 August 1999 相似文献
15.
Hayase Shisa Lingmin Lu Hideki Katoh Atsuko Kawarai Jun-ichi Tanuma Yoshibumi Matsushima Hiroshi Hiai 《Mammalian genome》1997,8(5):324-327
A new set of rat RI strains consisting of 11 independent strains and 13 of their substrains was established by inbreeding
F2 rats between F344/DuCrj and LE/Stm. The strain distribution pattern was examined for 66 microsatellite loci, 8 biochemical
genetic markers, 2 histocompatibility loci, and 2 coat color genes. A rat salivary protein gene Spe1 was newly mapped on Chr 1.
Received: 13 August 1996 / Accepted: 23 December 1996 相似文献
16.
Daniel H. Moralejo Tomoe Ogino Min Zhu Kiyotaka Toide Suwen Wei Kaichun Wei Takahisa Yamada Akira Mizuno Kozo Matsumoto Kenji Shima 《Mammalian genome》1998,9(10):794-798
The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for obese-type, non-insulin-dependent diabetes mellitus
(NIDDM) in humans. The OLETF rat has poor capacity for pancreatic proliferation, which may be the critical pathogenetic event
in NIDDM development. Our investigation was designed to identify quantitative trait loci (QTLs) responsible for poor pancreatic
proliferation by examining compensatory proliferation of the pancreatic remnant after partial pancreatectomy and performing
a genome-wide scan in an F2 intercross obtained by mating the OLETF and the Fischer-344 (F344) rats. We identified a highly significant QTL on rat Chromosome
14 with a maximum lod score of 16.7, which accounts for 55% of the total variance. The QTL co-localizes with the gene encoding
cholecystokinin type A receptor (CCKAR) which is likely to mediate the trophic effect of cholecystokinin on pancreas and is defective in the OLETF rat.
Received: 3 March 1998 / Accepted: 18 June 1998 相似文献
17.
Karen A. Gould Tracy E. Strecker Kimberly K. Hansen Kimberly K. Bynoté Kelli A. Peterson James D. Shull 《Mammalian genome》2006,17(5):451-464
Chronic estrogen administration can lead to thymic atrophy in rodents. In this article we report that the Brown Norway (BN)
rat is sensitive to thymic atrophy induced by the estrogen diethylstilbestrol (DES). By contrast, DES does not induce significant
thymic atrophy in the August × Copenhagen-Irish (ACI) strain. The sensitivity of the BN rat to DES-induced thymic atrophy
appears to segregate as an incompletely dominant trait in crosses between the BN and ACI strains. In a (BN × ACI)F2 population, we find strong evidence for three major genetic determinants of sensitivity to DES-induced thymic atrophy on
rat Chromosome (RNO) 10 and RNO2. Genotypes at these loci, termed Esta1, 2, and 3, do not have a significant impact on the ability of DES to induce pituitary tumorigenesis or inhibit growth of these F2 rats. These data indicate that the genetic factors that control DES-induced thymic atrophy are distinct from those that control
the effects of DES on pituitary mass and body mass. The Esta intervals on RNO10 and RNO2 overlap with loci that control sensitivity to radiation-induced thymocyte apoptosis, as well
as susceptibility to a variety of allergic and autoimmune pathologies, including allergic encephalitis, arthritis, and glomerulonephritis
in rodents. These observations suggest that common genetic determinants may control sensitivity to estrogen-induced thymic
atrophy, maintenance of thymocyte homeostasis, and immune function. 相似文献
18.
Quantitative trait loci for baseline white blood cell count, platelet count, and mean platelet volume 总被引:3,自引:0,他引:3
Luanne L. Peters Weidong Zhang Amy J. Lambert Carlo Brugnara Gary A. Churchill Orah S. Platt 《Mammalian genome》2005,16(10):749-763
A substantial genetic contribution to baseline peripheral blood counts has been established. We performed quantitative trait
locus/loci (QTL) analyses to identify chromosome (Chr) regions harboring genes influencing the baseline white blood cell (WBC)
count, platelet (Plt) count, and mean platelet volume (MPV) in F2 intercrosses between NZW/LacJ, SM/J, and C57BLKS/J inbred mice. We identified six significant WBC QTL: Wbcq1 (peak LOD score at 38 cM, Chr 1), Wbcq2 (42 cM, Chr 3), Wbcq3 (0 cM, Chr 15), Wbcq4 (58 cM, Chr 1), Wbcq5 (82 cM, Chr 1), and Wbcq6 (8 cM, Chr 14). Three significant Plt QTL were identified: Pltq1 (24 cM, Chr 2), Pltq2 (36 cM, Chr 7), and Pltq3 (10 cM, Chr 12). Two significant MPV QTL were identified, Mpvq1 (62 cM, Chr 15) and Mpvq2 (44 cM, Chr 8). In total, the WBC QTL accounted for up to 31% of the total variance in baseline WBC count, while the Plt
and MPV QTL accounted for up to 30% and 49% of the total variance, respectively. These analyses underscore the genetic complexity
underlying these traits in normal populations and provide the basis for future studies to identify novel genes involved in
the regulation of mammalian hematopoiesis. 相似文献
19.
Y. Du E. F. Remmers H. Zha E. A. Goldmuntz J. Szpirer C. Szpirer R. L. Wilder 《Mammalian genome》1995,6(4):295-298
Nine microsatellite loci were mapped to rat Chromosome (Chr) 7 by genetic linkage and somatic cell hybrid analysis. These loci include the gene encoding a member of the IID sub-family of cytochrome P450 (Cyp2d), a gene with repetitive sequences expressed during myotube formation (D7Arb1e), four anonymous loci, D7Arb81, D7Arb208, D7Arb569, D7Arb609a, and three DNA loci defined by MapPairTM markers R245, R513, and R1071. The nine loci were all identified by PCR-based microsatellite polymorphism analysis and were characterized in 40 F2 intercross progeny of Fischer (F344/N) and Lewis (LEW/N) rats for segregation analysis. These markers formed a single linkage group spanning 76.8 cM with the following order and distances: D7Arb569-11.4 cM-D7Arb81-9.7 cM-R513-2.6 cM-Cyp2d-0.0 cM-R245-1.3 cM-D7Arb1e-10.4 cM-R1071-15.9 cM-D7Arb609a-15.4 cM-D7Arb208. Physical mapping of Cyp2d by somatic cell hybrid analysis allowed us to assign this linkage group to rat Chr 7. For each marker, two to six alleles were detected in a panel of 16 inbred rat strains (ACI/N, BN/SsN, BUF/N, DA/Bkl, F344/N, LER/N, LEW/N, LOU/MN, MNR/N, MR/N, SHR/N, SR/Jr, SS/Jr, WBB1/N, WBB2/N, WKY/N). 相似文献
20.
Linkage map of seven polymorphic markers on rat Chromosome 18 总被引:8,自引:0,他引:8
Elaine F. Remmers Ellen A. Goldmuntz Hongbin Zha Leslie J. Crofford Joseph M. Cash Peter Mathern Ying Du Ronald L. Wilder 《Mammalian genome》1993,4(5):265-270
A genetic linkage map of seven polymorphic markers was created with F2 intercross progeny of F344/N and LEW/N rats and assigned to rat Chromosome (Chr) 18. Five of the markers described were defined by simple sequence length polymorphisms (SSLPs) associated with five genes: transthyretin (TTR), trypsin inhibitor-like protein (TILP), 2 adrenergic receptor (ADRB2), olfactory neuron-specific G protein (OLF), and gap junction protein (GJA1). One marker was defined by a restriction fragment length polymorphism (RFLP) detected with a probe for the human colony stimulating factor 1 receptor (CSF1R) gene. The D18N1R locus was defined by an anonymous DNA fragment amplified by the randomly amplified polymorphic DNA (RAPD) technique with a single short primer. These seven DNA loci formed a single genetic linkage group 30.4 cM in length with the following order: TTR-6.8 cM-D18N1R-9.1 cM-TILP-4.3 cM-CSF1R-0 cM-ADRB2-10.2 cM-OLF-0 cM-GJA1. The five SSLP markers were highly polymorphic. In a total of 13 inbred rat strains analyzed (F344/ N, LEW/N, LOU/MN, WBB1/N, WBB2/N, MR/N, MNR/N, ACI/N, SHR/N, WKY/N, BN/SsN, BUF/N, and LER/N), three to six alleles were detected for each marker. Remarkable linkage conservation was detected between the region of rat Chr 18 mapped and a region of mouse Chr 18. However, genes associated with these markers have been mapped to three different human chromosomes (Chrs 5, 6, and 18). The markers described here should be useful for genetic mapping studies and genetic monitoring of inbred rat strains. 相似文献