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1.
Kathryn Gill Nicolas Desaulniers Paule Desjardins Kristine Lake 《Mammalian genome》1998,9(12):929-935
The purpose of the present study was to characterize the C57BL/6J, A/J, and AXB/BXA Recombinant Inbred (RI) strains of mice
for voluntary alcohol consumption. Quantitative Trait Locus (QTL) analysis was used to provide provisional location of QTLs
for alcohol consumption. The inbred strains were screened for levels of alcohol intake (calculated as alcohol preference and
absolute alcohol consumption) by receiving 4 days of forced exposure to a 10% (wt/vol) solution of alcohol, followed by 3
weeks of free choice between water and 10% alcohol. A wide and continuous distribution of values for alcohol consumption and
preference was obtained in the AXB/BXA RI strains, confirming polygenic influences on alcohol-related behaviors. Significant
gender differences were found for both alcohol preference [F28,651= 2.12, p < 0.001] and absolute alcohol consumption [F28,647= 2.57, p < 0.001]. In males, putative QTLs were mapped to chromosomes (Chrs) 2, 5, 7, 10, 11, and 16. Multiple regression analysis
indicated that approximately 75% of the genetic variance in alcohol preference in males could be accounted for by three of
the QTL regions. Several of the putative QTLs appeared to be male-specific (Tyr on Chr 7; D10Mit126 on Chr 10; D11Mit61 on Chr 11). In females, seven putative QTLs were mapped to Chrs 2, 4, 5, 7, 11, 16, and 19. Approximately 90% of the genetic
variance in alcohol preference in females could be accounted for by four QTL regions, as determined by multiple regression.
The QTL on Chr 11 near D11Mit35 appeared to be female-specific. This site was close to a female-specific QTL (Alcp2) previously mapped in C57BL/6J × DBA/2J backcrosses by Melo and coworkers (Nat Genet 13, 147, 1996). The QTLs mapped for
alcohol preference in the present study must be considered suggestive at the present time, since only D2Mit74 met very strict statistical criteria for significance. However, the concordance across several studies for the loci on Chrs
2, 4, 7, 9, and 11 suggest that some common QTLs influencing alcohol preference have been identified. Confirmation of QTLs
mapped in the present study is currently being conducted in a new series of recombinant congenic (RC) strains developed from
reciprocal backcrosses between the A/J and C57BL/6J progenitors. The concomitant use of both RI and RC strains developed from
the same progenitors should provide a powerful means of detecting, confirming, and mapping QTLs for alcohol-related traits.
Received: 25 August 1998 / Accepted: 8 October 1998 相似文献
2.
T. N. Ferraro G. T. Golden G. G. Smith N. J. Schork P. St. Jean C. Ballas H. Choi W. H. Berrettini 《Mammalian genome》1997,8(3):200-208
Mature DBA/2J (D2) mice are very sensitive to seizures induced by various chemical and physical stimuli, whereas C57BL/6J
(B6) mice are relatively seizure resistant. We have conducted a genome-wide search for quantitative trait loci (QTLs) influencing
the differential sensitivity of these strains to kainic acid (KA)-induced seizures by studying an F2 intercross population. Parental, F1, and F2 mice (8–10 weeks of age) were injected subcutaneously with 25 mg/kg of KA and observed for 3 h. Latencies to focal and generalized
seizures and status epilepticus were recorded and used to calculate an overall seizure score. Results of seizure testing indicated
that the difference in susceptibility to KA-induced seizures between D2 and B6 mice is a polygenic phenomenon with at least
65% of the variance due to genetic factors. First-pass genome screening (10-cM marker intervals) in F2 progeny (n = 257) documented a QTL of moderate effect on Chromosome (Chr) 1 with a peak LOD score of 5.5 (17% of genetic
variance explained) localized between D1Mit30 and D1Mit16. Provisional QTLs of small effect were detected on Chr 11 (D11Mit224–D11Mit14), 15 (D15Mit6–D15Mit46) and 18 (D18Mit9–D18Mit144). Multiple locus models generally confirmed the Mapmaker/QTL results and also provided evidence for another QTL on Chr 4
(D4Mit9). Multilocus analysis of seizure severity suggested that additional loci on Chrs 5 (D5Mit11), 7 (D7Mit66), and 15 (D15Nds2) might also contribute to KA-induced seizure response. Overall, our results document a complex genetic determinism for KA-induced
seizures in these mouse strains with contributions from as many as eight QTLs.
Received: 16 April 1996 / Accepted: 21 October 1996 相似文献
3.
Elizabeth P. Blankenhorn Gregory Bryan Andrew V. Kossenkov Lise Desquenne Clark Xiang-Ming Zhang Celia Chang Wenhwai Horng L. Susan Pletscher James M. Cheverud Louise C. Showe Ellen Heber-Katz 《Mammalian genome》2009,20(11-12):720-733
MRL mice display unusual healing properties. When MRL ear pinnae are hole punched, the holes close completely without scarring, with regrowth of cartilage and reappearance of both hair follicles and sebaceous glands. Studies using (MRL/lpr × C57BL/6)F2 and backcross mice first showed that this phenomenon was genetically determined and that multiple loci contributed to this quantitative trait. The lpr mutation itself, however, was not one of them. In the present study we examined the genetic basis of healing in the Large (LG/J) mouse strain, a parent of the MRL mouse and a strain that shows the same healing phenotype. LG/J mice were crossed with Small (SM/J) mice and the F2 population was scored for healing and their genotypes determined at more than 200 polymorphic markers. As we previously observed for MRL and (MRL × B6)F2 mice, the wound-healing phenotype was sexually dimorphic, with female mice healing more quickly and more completely than male mice. We found quantitative trait loci (QTLs) on chromosomes (Chrs) 9, 10, 11, and 15. The heal QTLs on Chrs 11 and 15 were linked to differential healing primarily in male animals, whereas QTLs on Chrs 9 and 10 were not sexually dimorphic. A comparison of loci identified in previous crosses with those in the present report using LG/J × SM/J showed that loci on Chrs 9, 11, and 15 colocalized with those seen in previous MRL crosses, whereas the locus on Chr 10 was not seen before and is contributed by SM/J. 相似文献
4.
On the basis of eight independent quantitative trait loci (QTL) studies of ethanol (alcohol) preference drinking in mice,
a meta-analysis was carried out to examine the replicability of QTLs across studies and to enhance the power of QTL detection
and parameter estimation. To avoid genetic heterogeneity, we analyzed only studies of mapping populations derived from the
C57BL/6 (B6) and DBA/2 (D2) inbred progenitor strains. Because these studies were carried out in five different laboratories,
there were substantial differences in testing procedure, data analysis, and especially in the choice of mapping population
(BXD recombinant inbred strains, F2, backcross, selected lines, or congenic strains). Despite this, we found several QTLs that were sufficiently robust as to
appear consistently across studies given the strengths and weaknesses of the mapping populations employed. These were on Chromosomes
(Chrs) 2 (proximal to mid), 3 (mid to distal), 4 (distal), and 9 (proximal to mid). The P value for each of these QTLs, combined across all applicable studies, ranged from 10−7 to 10−15, with the additive effect of each QTL accounting for 3–5% of the trait variance extrapolated to an F2 population. Two other QTLs on Chrs 1 (distal) and 11 (mid) were less consistent, but still reached overall significance (P < .0001).
Received: 18 April 2001 / Accepted: 25 July 2001 相似文献
5.
Rea Victoria P Anunciado Masahiko Nishimura Masayuki Mori Akira Ishikawa Shin Tanaka Fumihiko Horio Tamio Ohno Takao Namikawa 《Experimental Animals》2003,52(1):37-42
Quantitative trait locus (QTL) analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels at 10 weeks of age was performed in 321 F2 offspring from SM/J and A/J mice. Interval mapping revealed a total of 22 suggestive QTLs affecting the four traits: two insulin QTLs on Chromosomes (Chrs) 6 and 8; six triglyceride QTLs on Chrs 4, 8, 9, 11, 12 and 19; six total-cholesterol QTLs on Chrs 1, 3, 4, 14, 17 and 19; and eight phospholipid QTLs on Chrs 2, 3, 4, 6, 8, 10 and 19. Gender influenced the expression of eight of the suggestive QTLs. The total-cholesterol QTLs on Chrs 4, 14 and 17, the triglyceride QTL on Chr 9 and the phospholipid QTL on Chr 4 were specific to females. The phospholipid QTLs on Chrs 2 and 6 and the insulin QTL on Chr 8 were specific to males. In addition, common QTLs involved in the regulation of some of the traits were identified. The female-specific QTL on Chr 4 appeared to be involved in the regulation of total cholesterol and phospholipid levels. The QTL on Chr 8 affected insulin and phospholipid levels, whereas the Chr 19 QTL was common to the three lipid parameters. 相似文献
6.
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
7.
A genome-wide scan for quantitative trait loci (QTLs) controlling body weight at 10 weeks after birth was carried out in
a population of 387 intersubspecific backcross mice derived from a cross between C57BL/6J inbred mice (Mus musculus domesticus) and wild mice (M. m. castaneus) captured in the Philippines, in order to discover novel QTLs from the wild mice that have about 60% lower body weight than
C57BL/6J. By interval mapping, we detected four QTLs: a highly significant QTL on Chromosome (Chr) 2, which was common in
both sexes; two significant QTLs on Chr 13, one male-specific and the other female-specific; and a suggestive male-specific
QTL on X Chr. By composite interval mapping, we confirmed the presence of the three QTLs on Chrs 2 and 13, but not of the
male-specific X-linked QTL. The composite interval mapping analysis newly identified three QTLs: a significant male-specific
QTL on Chr 11 and two highly significant female-specific QTLs on Chrs 9 and X. Individual QTLs explained 3.8–11.6% of the
phenotypic variance, and all the QTL alleles derived from the wild mice decreased body weight. A two-way analysis of variance
revealed a significant epistatic interaction between the Chr 2 QTL and the background marker locus D12Mit4 on Chr 12 only in males. The interaction effect unexpectedly increased body weight. The chromosomal region containing the
Chr 2 QTL did not coincide with those of growth or fatness QTLs mapped in previous studies. These results suggest that a population
of wild mice may play an important role as new sources of valuable QTLs.
Received: 14 January 2000 / Accepted: 14 April 2000 相似文献
8.
Eri Nishihara Shirng-Wern Tsaih Chieko Tsukahara Sarah Langley Susan Sheehan Keith DiPetrillo Satoshi Kunita Ken-ichi Yagami Gary A. Churchill Beverly Paigen Fumihiro Sugiyama 《Mammalian genome》2007,18(8):573-583
In a previous study in 15 inbred mouse strains, we found highest and lowest systolic blood pressures in NZO/HILtJ mice (metabolic
syndrome) and C3H/HeJ mice (common lean strain), respectively. To identify the loci involved in hypertension in metabolic
syndrome, we performed quantitative trait locus (QTL) analysis for blood pressure with direction of cross as a covariate in
segregating F2 males derived from NZO/HILtJ and C3H/HeJ mice. We detected three suggestive main-effect QTLs affecting systolic and diastolic
blood pressures (SBP and DBP). We analyzed the first principle component (PC1) generated from SBP and DBP to investigate blood
pressure. In addition to all the suggestive QTLs (Chrs 1, 3, and 8) in SBP and DBP, one suggestive QTL on Chr 4 was found
in PC1 in the main scan. Simultaneous search identified two significant epistatic locus pairs (Chrs 1 and 4, Chrs 4 and 8)
for PC1. Multiple regression analysis revealed three blood pressure QTLs (Bpq10, 100 cM on Chr 1; Bpq11, 6 cM on Chr 4; Bpq12, 29 cM on Chr 8) accounting for 29.4% of blood pressure variance. These were epistatic interaction QTLs constructing a small
network centered on Chr 4, suggesting the importance of genetic interaction for development of hypertension. The blood pressure
QTLs on Chrs 1, 4, and 8 were detected repeatedly in multiple studies using common inbred nonobese mouse strains, implying
substantial QTL independent of development of obesity and insulin resistance. These results enhance our understanding of complicated
genetic factors of hypertension in metabolic diseases.
Eri Nishihara, Shirng-Wern Tsaih, Chieko Tsukahara and Sarah Langley contributed equally to this work. 相似文献
9.
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
10.
Amy F. Eisener-Dorman Laura Grabowski-Boase Brian M. Steffy Tim Wiltshire Lisa M. Tarantino 《Mammalian genome》2010,21(5-6):231-246
Quantitative trait locus (QTL) mapping in the mouse typically utilizes inbred strains that exhibit significant genetic and phenotypic diversity. The development of dense SNP panels in a large number of inbred strains has eliminated the need to maximize genetic diversity in QTL studies as plenty of SNP markers are now available for almost any combination of strains. We conducted a QTL mapping experiment using both a backcross (N2) and an intercross (F2) between two genetically similar inbred mouse strains: C57BL/6J (B6) and C57L/J (C57). A set of additive QTLs for activity behaviors was identified on Chrs 1, 9, 13, and 15. We also identified additive QTLs for anxiety-related behaviors on Chrs 7, 9, and 16. A QTL on Chr 11 is sex-specific, and we revealed pairwise interactions between QTLs on Chrs 1 and 13 and Chrs 10 and 18. The Chr 9 activity QTL accounts for the largest amount of phenotypic variance and was not present in our recent analysis of a B6 × C58/J (C58) intercross (Bailey et al. in Genes Brain Behav 7:761–769, 2008). To narrow this QTL interval, we used a dense SNP haplotype map with over 7 million real and imputed SNP markers across 74 inbred mouse strains (Szatkiewicz et al. in Mamm Genome 19(3):199–208, 2008). Evaluation of shared and divergent haplotype blocks among B6, C57, and C58 strains narrowed the Chr 9 QTL interval considerably and highlights the utility of QTL mapping in closely related inbred strains. 相似文献
11.
Tohru Suzuki Akira Ishikawa Takashi Yoshimura Takao Namikawa Hiroshi Abe Sato Honma Ken-ichi Honma Shizufumi Ebihara 《Mammalian genome》2001,12(4):272-277
CS mice show a free-running period (κ) longer than 24 h and rhythm splitting in constant darkness (DD). These features in
behavioral circadian rhythms are distinctive as compared with other inbred strains of mice, which exhibit robust free-running
rhythms with κ shorter than 24 h. To identify the genes affecting κ, quantitative trait locus (QTL) analysis was initially
conducted by using 289 F2 mice derived from a cross between CS and C57BL/6J strain. A suggestive QTL (LOD = 3.71) with CS allele increasing κ was detected
on the distal region of Chromosome (Chr) 19. Next, using 192 F2 mice from a cross between CS and MSM strain, the presence of the QTL on Chr 19 was examined, and we confirmed the QTL at
the genome-wide significant level (LOD = 4.61 with 10.4% of the total variance explained). This QTL was named long free-running
period (Lfp). Three other suggestive QTLs (LOD = 3.24–4.28) were mapped to the midportion of Chr 12 in (CS×C57BL/6J)F2 mice, and to the proximal and middle region of Chr 19 in (CS×MSM)F2 mice, respectively, of which, CS alleles for two QTLs on Chr 19 have the effect of lengthening κ. None of these QTLs were
mapped to the chromosomal regions of previously described QTLs for κ and known clock genes (Clock, mPer1, Bmal1, mCry1, mCry2, mTim, and Csnk1e).
Received: 5 July 2000 / Accepted: 5 December 2000 相似文献
12.
Nakao R Kameda Y Kouguchi H Matsumoto J Dang Z Simon AY Torigoe D Sasaki N Oku Y Sugimoto C Agui T Yagi K 《International journal for parasitology》2011,41(11):1121-1128
Alveolar echinococcosis (AE) is a severe hepatic disorder caused by larval infection by the fox tapeworm Echinococcus multilocularis. The course of parasitic development and host reactions are known to vary significantly among host species, and even among different inbred strains of mice. As reported previously, after oral administration of parasite eggs, DBA/2 (D2) mice showed a higher rate of cyst establishment and more advanced protoscolex development in the liver than C57BL/6 (B6) mice. These findings strongly suggest that the outcome of AE is affected by host genetic factor(s). In the present study, the genetic basis of such strain-specific differences in susceptibility/resistance to AE in murine models was studied by whole-genome scanning for quantitative trait loci (QTLs) using a backcross of (B6 × D2)F1 and D2 mice with varying susceptibility to E. multilocularis infection. For cyst establishment, genome linkage analysis identified one suggestive and one significant QTL on chromosomes (Chrs.) 9 and 6, respectively, whereas for protoscolex development, two suggestive and one highly significant QTLs were detected on Chrs. 6, 17 and 1, respectively. Our QTL analyses using murine AE models revealed that multiple genetic factors regulated host susceptibility/resistance to E. multilocularis infection. Moreover, our findings show that establishment of the parasite cysts in the liver is affected by QTLs that are distinct from those associated with the subsequent protoscolex development of the parasite, indicating that different host factors are involved in the host–parasite interplay at each developmental stage of the larval parasite. Further identification of responsible genes located on the identified QTLs could lead to the development of effective disease prevention and control strategies, including an intensive screening and clinical follow-up of genetically high-risk groups for AE infection. 相似文献
13.
Michael Danciger Michael T. Matthes Douglas Yasamura Novrouz B. Akhmedov Tammy Rickabaugh Susan Gentleman T. Michael Redmond Matthew M. La Vail Debora B. Farber 《Mammalian genome》2000,11(6):422-427
C57BL/6J-c2J (c2J) albino mice showed much less damage to their photoreceptors after exposure to prolonged light than BALB/c mice and
seven other albino strains tested. There were no gender differences, and preliminary studies suggested that the c2J relative
protective effect was a complex trait. A genome-wide scan using dinucleotide repeat markers was carried out for the analysis
of 194 progeny of the backcross (c2J × BALB/c)F1× c2J and the thickness of the outer nuclear layer (ONL) of the retina was the quantitative trait reflecting retinal damage.
Our results revealed a strong and highly significant quantitative trait locus (QTL) on mouse Chromosome (Chr) 3 that contributes
almost 50% of the c2J protective effect, and three other very weak but significant QTLs on Chrs 9, 12, and 14. Interestingly,
the Chrs 9 and 12 QTLs corresponded to relative susceptibility alleles in c2J (or relative protection alleles in BALB/c),
the opposite of the relative protective effect of the QTLs on Chrs 3 and 14. We mapped the Rpe65 gene to the apex of the Chr 3 QTL (LOD score = 19.3). Northern analysis showed no difference in retinal expression of Rpe65 message between c2J and BALB/c mice. However, sequencing of the Rpe65 message revealed a single base change in codon 450, predicting a methionine in c2J and a leucine in BALB/c.
When the retinas of aging BALB/c and c2J mice reared in normal cyclic light were compared, the BALB/c retinas showed a small
but significant loss of photoreceptor cells, while the c2J retinas did not. Finding light damage-modifying genes in the mouse
may open avenues of study for understanding age-related macular degeneration and other retinal degenerations, since light
exposures may contribute to the course of these diseases.
Received: 14 December 1999 / Accepted: 18 February 2000 相似文献
14.
A genome-wide scan was performed in order to identify Quantitative Trait Loci (QTL) associated with growth in a population
segregating high growth (hg), a partially recessive mutation that enhances growth rate and body size in the mouse. A sample of 262 hg/hg mice was selected from a C57BL/6J-hg/hg× CAST/EiJ F2 cross and typed with 79 SSLP markers distributed across the genome. Eight significant loci were identified through interval
mapping. Loci on Chromosomes (Chrs) 2 and 8 affected the growth rate of F2 mice. Loci on Chr 2 and 11 affected growth rate and carcass lean mass (protein and ash). A locus on Chr 9 modified femur
length and another one in Chr 17 affected both carcass lean mass and femur length, but none of these had significant effects
on growth rate. Loci on Chrs 5 and 9 modified carcass fat content. Additive effects were positive for C57BL/6J alleles, except
for the two loci affecting carcass fatness. Typing of selected markers in 274 +/+ F2 mice revealed significant interactions between hg and other growth QTL, which were detected as changes in gene action (additive or dominant) and in allele substitution effects.
Knowledge about interactions between loci, especially when major genes are involved, will help in the identification of positional
candidate genes and in the understanding of the complex genetic regulation of growth rate and body size in mammals.
Received: 29 June 2000 / Accepted: 22 November 2000 相似文献
15.
Yuka Namiki Yasuhiro Kon Katsuyuki Kazusa Atsushi Asano Nobuya Sasaki Takashi Agui 《Mammalian genome》2005,16(2):96-102
The MRL/MpJ mouse has previously been reported to possess an interesting phenotype in which spermatocytes are resistant to the abdominal temperature heat shock. In this study genetic analysis for it was performed. The phenotypes of F2 progenies produced by mating MRL/MpJ and control strain C57BL/6 mice were not segregated into two types as parental phenotypes, suggesting that the phenotype is controlled by multiple genetic loci. Thus, quantitative trait loci (QTL) analysis was performed using 98 microsatellite markers. The weight ratio of the cryptorchid testis to the intact testis (testis weight ratio) and the Sertoli cell index were used for quantitative traits. QTL analysis revealed two significant QTLs located on Chrs 1 and 11 for testis weight ratio and one significant QTL located in the same region of Chr 1 for the Sertoli cell index. A microsatellite marker locus located in the peak of the QTL on Chr 1 did not recombine with the exonuclease 1 (Exo1) gene locus in 140 F2 progenies. Mutation of the Exo1 gene was previously reported to be responsible for metaphase-specific apoptosis (MSA) of spermatocytes in the MRL/MpJ mouse. These results raise the possibility that mutation of the Exo1 gene is responsible for both MSA and heat stress resistance of spermatocytes in the MRL/MpJ mouse. 相似文献
16.
K. E. Samocha J. E. Lim R. Cheng G. Sokoloff A. A. Palmer 《Genes, Brain & Behavior》2010,9(7):759-767
Prepulse inhibition (PPI) of the startle response is a measure of sensorimotor gating, a process that filters out extraneous sensory, motor and cognitive information. Humans with neurological and psychiatric disorders, including schizophrenia, obsessive‐compulsive disorder and Huntington's disease, exhibit a reduction in PPI. Habituation of the startle response is also disrupted in schizophrenic patients. In order to elucidate the genes involved in sensorimotor gating, we phenotyped 472 mice from an F2 cross between LG/J × SM/J for PPI and genotyped these mice genome‐wide using 162 single nucleotide polymorphism (SNP) markers. We used prepulse intensity levels that were 3, 6 and 12 dB above background (PPI3, PPI6 and PPI12, respectively). We identified a significant quantitative trait locus (QTL) on chromosome 12 for all three prepulse intensities as well as a significant QTL for both PPI6 and PPI12 on chromosome 11. We identified QTLs on chromosomes 7 and 17 for the startle response when sex was included as an interactive covariate and found a QTL for habituation of the startle response on chromosome 4. We also phenotyped 135 mice from an F34 advanced intercross line (AIL) between LG/J × SM/J for PPI and genotyped them at more than 3000 SNP markers. Inclusions of data from the AIL mice reduced the size of several of these QTLs to less than 5 cM. These results will be useful for identifying genes that influence sensorimotor gaiting and show the power of AIL for fine mapping of QTLs. 相似文献
17.
To determine the genetic variation that contributes to body composition in the mouse, we interbred a wild-derived strain (PWK/PhJ;
PWK) with a common laboratory strain (C57BL/6J; B6). The parental, F1, and F2 mice were phenotyped at 18 weeks old for body weight and composition using dual-energy X-ray absorptiometry (DEXA). A total
of 479 (244 male and 235 female) F2 mice were genotyped for 117 polymorphic markers spanning the autosomes. Twenty-eight suggestive or significant linkages for
four traits (body weight, adjusted lean and fat weight, and percent fat) were detected. Of these, three QTLs were novel: one
on the proximal portion of Chr 5 for body weight (Bwq8; LOD = 4.7), one on Chr 3 for lean weight (Bwtq13; LOD = 3.6), and one on Chr 11 for percent fat (Adip19; LOD = 5.8). The remaining QTLs overlapped previously identified linkages, e.g., Adip5 on Chr 9. One QTL was sex-specific (present in males only) and seven were sex-biased (more prominent in one sex than the
other). Most alleles that increased body weight were contributed by the B6 strain, and most alleles that increased percent
fat were contributed by the PWK strain. Eight pairs of interacting loci were identified, none of which exactly overlapped
the main-effect QTLs. Many of the QTLs found in the B6 × PWK cross map to the location of previously reported linkages, suggesting
that some QTLs are common to many strains (consensus QTLs), but three new QTLs appear to be particular to the PWK strain.
The location and type of QTLs detected in this new cross will assist in future efforts to identify the genetic variation that
determines the ratio of lean to fat weight as well as body size in mice. 相似文献
18.
Male F1 hybrids between inbred strains and Mus macedonicus have very small testes and are sterile. Cytological analysis of testes shows very few meioses. To determine the genetic basis for this sterility, (C57BL/6J × Mus macedonics) F1 females were mated to males from C57BL/10J. In about half the male progeny no meiosis I was observed. About half of the animals that progressed through meiosis I showed other indications of low fertility and the balance appeared fertile. QTL analysis of the progeny suggested that loci on proximal Chrs 17 and X were involved in the sterility and a locus on Chr X in variation of body weight. There is also evidence that X//Y dissociation of the pseudo-autosomal region occurs. The QTLs on Chrs X and 17 together account for about 37% of the variance for testis weight. Congenic lines B.MAC-X(1-38), and B.MAC-17(1-23) have been constructed using a modified speed congenic approach. Testis tubules from B.MAC-X(1-38) are narrow and vacuolated. They contain only Sertoli cells and mitotically dividing spermatogonia. Very occasionally a meiotic metaphase can be observed, but no sperm are produced. Homozygous males from B.MAC-17(1-23) are sterile, producing sperm heads but no complete sperm. 相似文献
19.
Jun-ichi Suto Saori Matsuura Kenkichi Imamura Harumichi Yamanaka Kenji Sekikawa 《Mammalian genome》1998,9(7):506-510
KK mouse is known as a polygenic model for non-insulin-dependent diabetes mellitus with moderate obesity. To identify the
quantitative trait loci (QTLs) responsible for the body weight in KK, linkage analysis with 97 microsatellite markers was
carried out into 192 F2 progeny, comprising 93 mice with a/a genotype at agouti locus and 99 mice with A
y
/a genotype, of a cross between C57BL/6J female and KK-Ay (Ay congenic) male, thereby the influence of A
y
allele on the quantitative regulation of body weight was also examined. In F2
a/a mice, we identified a QTL on Chromosome (Chr) 4, and two loci with suggestive linkage on Chrs 15 and 18. In F2
A
y
/a mice, a QTL was identified on Chr 6, and two loci with suggestive linkage were identified on Chrs 4 and 16. That the QTL
on Chr 4 was held in common between F2
a/a and F2
A
y
/a progenies implies that this locus may be a primary component regulating body weight in KK and KK-Ay. These results suggest that the body weight in KK is controlled by multiple genes, and the different combination of loci
is involved in the presence of A
y
allele. The QTL on Chr 6 seemed to determine the body weight by controlling fat deposition, because the linkage was identified
on body weight and adiposity, and is suggested to be a component involved in the metabolic pathway in obesity caused by the
A
y
allele.
Received: 16 December 1997 / Accepted: 16 March 1998 相似文献
20.
Masinde GL Li X Gu W Hamilton-Ulland M Mohan S Baylink DJ 《Functional & integrative genomics》2002,2(3):120-125
The genetic mechanisms that determine muscle size have not been elucidated, even though it is a key musculoskeletal parameter
that reflects muscle strength. In this study, we performed a high-density genome-wide scan using 633 (MRL/MPJ × SJL/J) F2 intercross 7-week-old mice to identify quantitative trait loci (QTL) involved in the determination of muscle size. Significant
QTL were identified for muscle size and body length. Muscle size (adjusted by body length) QTL were identified on chromosomes
7, 9, 11, 14 (two QTL) and 17, which together explained 19.2% of phenotypic variance in F2 mice, while body length QTL were located on chromosome 2 (two QTL), 9, 11 and 17 which accounted for 28.3% of phenotypic variance
in F2 mice. Three significant epistatic interactions between different QTL positions from muscle size and body length were identified
(P <0.01) on chromosomes 2, 9, 14 and 17, which explained 16.1% of the variance in F2 mice.
Electronic Publication 相似文献