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PubMed1999

Disease states associated with telomerase deficiency appear earlier in mice with short telomeres.

Mice deficient for the mouse telomerase RNA (mTR-/-) and lacking telomerase activity can only be bred for approximately six generations due to decreased male and female fertility and to an increased embryonic lethality associated with a neural tube closure defect. Although late generation mTR-/- mice show defects in the hematopoietic system, they are viable to adulthood, only showing a decrease in viability in old age. To assess the contribution of genetic background to the effect of telomerase deficiency on viability, we generated mTR-/- mutants on a C57BL6 background, which showed shorter telomeres than the original mixed genetic background C57BL6/129Sv. Interestingly, these mice could be bred for only four generations and the survival of late generation mTR-/- mice decreased dramatically with age as compared with their wild-type counterparts. Fifty percent of the generation 4 mice die at only 5 months of age. This decreased viability with age in the late generation mice is coincident with telomere shortening, sterility, splenic atrophy, reduced proliferative capacity of B and T cells, abnormal hematology and atrophy of the small intestine. These results indicate that telomere shortening in mTR-/- mice leads to progressive loss of organismal viability.

Aging↗
PubMed2004

Heterogeneity of the immune response to adenovirus-mediated factor VIII gene therapy in different inbred hemophilic mouse strains.

BACKGROUND: The development of anti-factor VIII (FVIII) antibodies (inhibitors) is a critical concern when considering gene therapy as a potential treatment modality for hemophilia A. We used a hemophilia A mouse model bred on different genetic backgrounds to explore genetically controlled differences in the immune response to FVIII gene therapy. METHODS: C57BL/6 FVIII knockout (C57-FVIIIKO) mice were bred with normal BALB/c (BAL) mice, to generate a recombinant congenic BAL-FVIIIKO model of hemophilia A. Early generation adenoviral (Ad) vectors containing the canine FVIII B-domain-deleted transgene under the control of either the CMV promoter or a tissue-restricted (TR) promoter were administered to C57-FVIIIKO, C57xBAL(F1)-FVIIIKO crosses, and BAL-FVIIIKO mice. FVIII expression, inhibitor development, inflammation, and vector-mediated toxicity were assessed. RESULTS: In response to administration of Ad-CMV-cFVIII, C57-FVIIIKO mice attain 3-fold higher levels of FVIII expression than BAL-FVIIIKO. All strains injected with Ad-CMV-FVIII displayed FVIII expression lasting only 2 weeks, with associated inhibitor development. C57-FVIII-KO mice that received Ad-TR-FVIII expressed FVIII for 12 months post-injection, whereas FVIII expression was limited to 1 week in C57xBAL(F1)-FVIIIKO and BAL-FVIIIKO mice. This loss of expression was associated with anti-FVIII inhibitor development. BAL-FVIIIKO mice showed increased hepatotoxicity with alanine aminotransferase levels reaching 4-fold higher levels than C57-FVIIIKO mice. However, C57-FVIIIKO mice initiate a more rapid and effective cell-mediated clearance of virally transduced cells than BAL-FVIIIKO, as evidenced by real-time PCR analysis of transduced tissues. Overall, strain-dependent differences in the immune response to FVIII gene delivery were only noted in the adaptive response, and not in the innate response. CONCLUSIONS: Our results indicate that the genetic background of the murine model of hemophilia A influences FVIII expression levels, the development of anti-FVIII inhibitors, clearance of transduced cells, and the severity of vector-mediated hepatotoxicity.

Adenoviridae↗
PubMed1999

Receptor-independent activators of heterotrimeric G-protein signaling pathways.

Heterotrimeric G-protein signaling systems are activated via cell surface receptors possessing the seven-membrane span motif. Several observations suggest the existence of other modes of stimulus input to heterotrimeric G-proteins. As part of an overall effort to identify such proteins we developed a functional screen based upon the pheromone response pathway in Saccharomyces cerevisiae. We identified two mammalian proteins, AGS2 and AGS3 (activators of G-protein signaling), that activated the pheromone response pathway at the level of heterotrimeric G-proteins in the absence of a typical receptor. beta-galactosidase reporter assays in yeast strains expressing different Galpha subunits (Gpa1, G(s)alpha, G(i)alpha(2(Gpa1(1-41))), G(i)alpha(3(Gpa1(1-41))), Galpha(16(Gpa1(1-41)))) indicated that AGS proteins selectively activated G-protein heterotrimers. AGS3 was only active in the G(i)alpha(2) and G(i)alpha(3) genetic backgrounds, whereas AGS2 was active in each of the genetic backgrounds except Gpa1. In protein interaction studies, AGS2 selectively associated with Gbetagamma, whereas AGS3 bound Galpha and exhibited a preference for GalphaGDP versus GalphaGTPgammaS. Subsequent studies indicated that the mechanisms of G-protein activation by AGS2 and AGS3 were distinct from that of a typical G-protein-coupled receptor. AGS proteins provide unexpected mechanisms for input to heterotrimeric G-protein signaling pathways. AGS2 and AGS3 may also serve as novel binding partners for Galpha and Gbetagamma that allow the subunits to subserve functions that do not require initial heterotrimer formation.

Amino Acid Sequence↗
PubMed2005

Roles of RAS and BRAF mutations in thyroid carcinogenesis.

Papillary carcinoma and follicular carcinoma are types of differentiated thyroid carcinomas, develop from the same thyroid follicular epithelial cells and show distinct biological behavior. Although several studies have demonstrated differences in the biological characteristics of these carcinomas, little is known about the genetic backgrounds that underlie these differences. The clarification of the genetic background can lead to the understanding of thyroid carcinogenesis, proper therapeutic strategies, and development of the molecular targeting drugs. Recently, aberrant activation of RAS-RAF-MEK-MAP kinase signaling pathway is frequently found in thyroid carcinoma. The pathway transmits a mitogenic signal to the nucleus, and constitutive activation of the pathway is thought to promote uncontrolled cell division. In our series, BRAF mutation was detected exclusively in papillary carcinoma (54%), and was exclusively V599E (a single nucleotide change of A-T at nucleotide 1796). NRAS mutation was observed in follicular carcinoma (50%) and in anaplastic carcinoma (28%), and was exclusively Q61R (a single nucleotide change of A-G at nucleotide 182). No mutations were found in KRAS or HRAS. In this chapter, we explain the role of RAS-RAF-MEK-MAP kinase pathway in carcinogenesis of the thyroid and its clinical implication based on our study. In addition, we review the current knowledge in this field.

Adenocarcinoma, Follicular↗
PubMed1996

[A genetic epidemiological study on lung cancer].

Segregation ratio, heritability and relative risk of genetic susceptibility were estimated for 355 families of lung cancer in matched pair with genetic epidemiological methods. Results showed that segregation ratio for lung cancer was 0.09-0.12 (95% confidence interval, CI) and heritability of lung cancer was (40.58 +/- 4.01)% and (27.58 +/- 4.76)% for smokers and non-smokers, respectively. Relative risks of genetic susceptibility to lung cancer were 4.73 (95% CI 3.90-5.74) and 2.61 (95% CI 2.18-3.13) in their first and second degree relatives, respectively, after adjustment of smoking with a logistic regression model. It was also found that there was an interaction between smoking habit and genetic background of lung cancer. Thus, it is believed that genetic background is one of the multifactorial causes in lung cancer.

China↗
PubMed2000

An epistatic interaction controls the latency of a transgene-induced mammary tumor.

Previous studies from our laboratory demonstrated that the latency, tumor growth, and metastatic progression of polyoma middle T-induced mammary tumor in an FVB/NJ inbred mouse background could be significantly altered by the introduction of different genetic backgrounds. In this study we extend these findings by mapping a number of interacting quantitative trait loci responsible for the changes in phenotype. Introduction of the I/LnJ inbred genetic background into the FVB/NJ-PyMT animal significantly accelerated the appearance of the primary tumor (35 vs. 57 days postnatal, p < 10(-7)). A backcross mapping panel was established, and loci responsible for the tumor acceleration were detected on Chrs 15 and 9. Examination of the genotype/phenotype correlation revealed that the FVB/NJ but not the I/LnJ allele of the Chr 15 locus was associated with tumor acceleration and was conditional on the presence of I/LnJ allele on Chr 9. These loci, designated Apmt1 and Apmt2, map to homologous regions associated with LOH in human breast cancer. These results suggest that allelic variants of genes in these regions may contribute to age of onset in human breast cancer.

Animals↗
PubMed2002

Extending the coalescent to multilocus systems: the case of balancing selection.

Natural populations are structured spatially into local populations and genetically into diverse 'genetic backgrounds' defined by different combinations of selected alleles. If selection maintains genetic backgrounds at constant frequency then neutral diversity is enhanced. By contrast, if background frequencies fluctuate then diversity is reduced. Provided that the population size of each background is large enough, these effects can be described by the structured coalescent process. Almost all the extant results based on the coalescent deal with a single selected locus. Yet we know that very large numbers of genes are under selection and that any substantial effects are likely to be due to the cumulative effects of many loci. Here, we set up a general framework for the extension of the coalescent to multilocus scenarios and we use it to study the simplest model, where strong balancing selection acting on a set of n loci maintains 2n backgrounds at constant frequencies and at linkage equilibrium. Analytical results show that the expected linked neutral diversity increases exponentially with the number of selected loci and can become extremely large. However, simulation results reveal that the structured coalescent approach breaks down when the number of backgrounds approaches the population size, because of stochastic fluctuations in background frequencies. A new method is needed to extend the structured coalescent to cases with large numbers of backgrounds.

Alleles↗
PubMed2000

Spontaneous thrombosis in mice carrying the factor V Leiden mutation.

A polymorphism in coagulation factor V, factor V Leiden (FVL), is the major known genetic risk factor for thrombosis in humans. Approximately 10% of mutation carriers experience clinically significant thrombosis in their lifetime. In a small subset of patients, thrombosis is associated with coinheritance of other prothrombotic gene mutations. However, the potential contribution of additional genetic risk factors in the majority of patients remains unknown. To gain insight into the molecular basis for the variable expressivity of FVL, mice were generated carrying the homologous mutation (R504Q [single-letter amino acid codes]) inserted into the endogenous murine Fv gene. Adult heterozygous (FvQ/+) and homozygous (FvQ/Q) mice are viable and fertile and exhibit normal survival. Compared with wild-type mice, adult FvQ/Q mice demonstrate a marked increase in spontaneous tissue fibrin deposition. No differences in fetal development or survival are observed among FvQ/Q, FvQ/+ or control littermates on the C57BL/6J genetic background. In contrast, on a mixed 129Sv-C57BL/6J genetic background, FvQ/Q mice develop disseminated intravascular thrombosis in the perinatal period, resulting in significant mortality shortly after birth. These results may explain the high degree of conservation of the R504/R506 activated protein C cleavage site within FV among mammalian species and suggest an important contribution of other genetic factors to the thrombosis associated with FVL in humans. (Blood. 2000;96:4222-4226)

Activated Protein C Resistance↗
PubMed2006

[RAPD analysis of Scutellaria baicalensis from different germplasms].

OBJECTIVE: To provide reference for breeding Scutellaria baicalensis from different germplasms,and to explore their genetic diversities and different strains. METHOD: The RAPD method was applied to the study on S. baicalensis from different germplasms by use of 14 random primers about 10 bp, and SAPD-analysis of 34 S. baicalensis from different germplasms was carried out by using the method of withingroups-linkage in SPSS 10.0. RESULTS: 14 among 115 primers were selected to amplify about 165 segments of DNA. Among them, 132 segments of DNA, 80.0% of the total, can represent genetic of diversities of S. baicalensis. According to RAPD analysis, 34 germplasms of S. baicalensis were classified into A, B, C and D categories. CONCLUSION: S. baicalensis from different germplasms shows abundant genetic diversities. Germplasms from Shandong like Mengyin 3, Menyin 2 and Pingyi have close distance (0.315) in genetic background, which can be chosen for breeding of cultivated. Though genetic characters are similar in the morphology, the geological distribution of S. baicalensis and its morphology have not certain correlation. The complex genetic background of S. baicalensis indicate that the work of the selective breeding and management for breeding of S. baicalensis have to be strengthened.

Breeding↗
PubMed2004

Genetic analysis of rice varietal diversity for rice blast control.

Two Indica hybrid rice of Shanyou63 (A) and Shanyou22 (B), two glutinous landraces of Huanghenuo (C) and Zinuo (D) and three improved Japonica rice of Hexi41 (E), Chujing12 (F) and 8126 (G) were selected and their genetic resistance relationship was estimated using resistance gene analogue (RGA). The results showed that there were similar genetic relationships between hybrid varieties at the genetic similarity (GS) of 0.86,and among improved Japonica varieties at the GS of 0.84, while highly genetic diversifications between traditional varieties, Indica and Japonica varieties, traditional and modern variety ( GS:0.45). The results also showed that clustering analysis based on RGA data were generally corresponded to known pedigrees and blast field resistances of the varieties. Based on varietal differences in RGA data and agronomic traits, plot experiments of five mixed-planting combinations of A/C, A/D, B/C, B/D and A/B and two combinations of E/C and E/F/G were conducted in Jianshui and Shiping counties ( Indica rice growing region) and Luxi County (warm Japonica region) in Yunnan Province in past two years, respectively. The results demonstrated that rice blast management was more effective in five mixed-planting combinations of varieties with different genetic backgrounds (GS: 0.45-0.77) than in two combinations with similar genetic relationships (GS: 0.84-0.90), compared with their monocultures. It is evident for the highly susceptible landraces in mixed-planting to achieve disease control, with significant decreases both in incidence and severity. The blast control efficiencies of landraces in different mixture combinations reached to 54.47%-92.18%. The control efficiencies of improved varieties varied from 15.12% to 25.54% in mixture combinations with closed genetic relationship. In addition,the total yield of 5 varietal combinations with distant genetic relationship increased 539.0-904.0 kg/ha in the mixed-planting plots, at increase rates of 5.6%-10.2%. Mixed rice varieties with similar genetic background did not achieve significant yield increase. Otherwise, the yield of E/F/G decreased 2.7%-4.0% compared with pure stand. The results can provide scientific basis of varietal combinations in diversification experiments for blast control.

Genetic Variation↗
PubMed2005

MHC-independent genetic regulation of liver damage in a mouse model of autoimmune hepatocellular injury.

Autoimmune hepatitis (AIH) is mediated by a T-cell attack upon liver parenchyma. Susceptibility to the development of AIH is genetically determined. While particular MHC haplotypes are known risk factors, it has been widely speculated that autoimmune liver damage can be regulated by additional genetic loci unlinked to MHC. However, evidence for the existence of such loci in humans is scant. We examined the contribution of the MHC in a murine model of autoimmune hepatocellular injury. BALB/c mice lacking the immunoregulatory cytokine transforming growth factor-beta1 (TGF-beta1) rapidly develop autoimmune T-helper 1-mediated necroinflammatory liver disease. Susceptibility to liver damage is strictly regulated by genetic background. Whereas TGF-beta1-deficient mice on the BALB/c background develop necroinflammatory liver disease, TGF-beta1-deficient mice on the 129/CF-1 genetic background do not. We asked whether MHC locus haplotype is the principal determinant of genetic susceptibility to liver disease in this model system. BALB/c mice harbor the H-2d haplotype. We used a 'haplotype swapping' approach to generate H-2b or H-2k congenic BALB-background TGF-beta1-deficient mice. In addition, F1 (BALB/c x 129/CF-1)-TGF-beta1-deficient mice were generated. As determined by plasma transaminase levels and histopathology, severe necroinflammatory liver disease developed in all BALB-background TGF-beta1-deficient mice, regardless of H-2 haplotype, but developed neither in 129/CF-1-TGF-beta1-deficient mice nor in F1 (BALB/c x 129/CF-1)-TGF-beta1-deficient mice. Thus, H-2d is neither necessary nor sufficient for the development of necroinflammatory liver disease in BALB-background TGF-beta1-deficient mice. This constitutes the first direct evidence that susceptibility to autoimmune hepatocellular damage, at least in mice, can be determined by genetic loci distinct from the MHC.

Alanine Transaminase↗
PubMed2005

Genetic evidence for a maternal effect locus controlling genomic imprinting and growth.

Crosses between two species of deer mouse (Peromyscus) yield dramatic parent-of-origin effects. Female P. maniculatus (BW) crossed with male P. polionotus (PO) produce animals smaller than either parent. PO females crossed with BW males yield lethal overgrowth that has been associated with loss-of-imprinting (LOI). Previously, we mapped two loci influencing fetal growth. These two loci, however, do not account for the LOI, nor for the dysmorphic phenotypes. Here we report that maternal genetic background strongly influences the LOI. Analyses of crosses wherein maternal genetic background is varied suggest that this effect is likely due to the action of a small number of loci. We have termed these putative loci Meil. Estimation of Meil loci number was confounded by skewed allelic ratios in the intercross line employed. We show that the Meil loci are not identical to any of the DNA methyltransferases shown to be involved in regulation of genomic imprinting.

Animals↗
PubMed1993

The hypertensive Y chromosome elevates blood pressure in F11 normotensive rats.

Our laboratory has shown that the Y chromosome has a significant effect on blood pressure in the spontaneously hypertensive rat (SHR) model of hypertension and that the testes and androgen receptor contribute to the blood pressure rise. As an extension of our research, we have developed two new rat strains, SHR/a and SHR/y (F11) to study the Y chromosome. The objectives of the following research were 1) to study the blood pressure of rats with an SHR Y chromosome in a normotensive genetic background (SHR/y) or a normotensive Y chromosome in an SHR genetic background (SHR/a), 2) to determine the effect of male sex phenotype on the blood pressure of these rats, 3) to determine if testosterone replacement in castrated rats would restore blood pressure, and 4) to determine whether the Y chromosome from the SHR/y strain when crossed with a normotensive female can induce hypertension in androgen receptor-deficient male offspring. Blood pressure of male SHR/y rats was significantly higher than that of normotensive Wistar-Kyoto males (p < 0.01), and SHR/a males had significantly lower blood pressure compared with that of the parent SHR strain (p = 0.05). Testosterone replacement in castrated rats of both strains (SHR/a and SHR/y) restored blood pressure to control levels. Normotensive female King-Holtzman rats heterozygous for the testicular feminization gene were crossed with F11 SHR/a and SHR/y males.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed2003

Fractal dynamics in circadian cardiac time series of corticotropin-releasing factor receptor subtype-2 deficient mice.

Non-linear fractal analysis of circadian 24 hr heartbeat interval time series was performed in corticotropin releasing factor receptor-subtype 2 (CRFR2) deficient mice. We hypothesized that, as a result of its central as well as its peripheral expression, CRFR2 would mediate or interfere with the circadian rhythmicity. The dynamical properties of cardiac interbeat intervals were expected to be different between CRFR2 (+/+) and CRFR2 (-/-) mice when studied over an extended circadian 24 hr cycle. The dynamics of neurocardiac control were found to remain remarkably stable throughout the circadian cycle. In disagreement with the initial hypothesis, the dynamical properties underlying the cardiac control process were common to both CRFR2 (+/+) and CRFR2 (-/-) mice suggesting that control of heart rate does not rely on the elaborate interaction of the CRFR2-sensor and its intrinsic feedback arrangement. Lack of expression of CRFR2 would not compromise cardiac control and its dynamical output or is subserved by other, unknown mechanisms. Functional integrity of CRFR2 would not constitute an indispensable requirement of physiologic cardiac control. The circadian rhythm of heart rate is generated centrally and is independent of expression of CRFR2. While 'normal' strain C57BL/6N mice exhibit a circadian dark/light cycle of heart rate, absence of circadian fluctuations in transgenic CRFR2-mice (both +/+ and -/-) and 'normal' strain C57BL/6J mice points at the importance of other deficiencies that may be related to a common genetic background. Mutant mice that share a common 129SvJ- or C57BL/6J-derived genetic background may not present an optimal model for physiological studies of cardiovascular control.

Algorithms↗
PubMed1998

mRNA surveillance mitigates genetic dominance in Caenorhabditis elegans.

Nonsense mutant mRNAs are unstable in all eucaryotes tested, a phenomenon termed nonsense-mediated mRNA decay (NMD) or mRNA surveillance. Functions of the seven smg genes are required for mRNA surveillance in Caenorhabditis elegans. In Smg(+) genetic backgrounds, nonsense-mutant mRNAs are unstable, while in Smg(-) backgrounds such mRNAs are stable. Previous work has demonstrated that the elevated level of nonsense-mutant mRNAs in Smg(-) animals can influence the phenotypic effects of heterozygous nonsense mutations. Certain nonsense alleles of a muscle myosin heavy chain gene are recessive in Smg(+) backgrounds but strongly dominant in Smg(-) backgrounds. Such alleles probably express disruptive myosin polypeptide fragments whose abundance is elevated in smg mutants due to elevation of mRNA levels. We report here that mutations in a variety of C. elegans genes are strongly dominant in Smg(-), but recessive or only weakly dominant in Smg(+) backgrounds. We isolated 32 dominant visible mutations in a Smg(-) genetic background and tested whether their dominance requires a functional NMD system. The dominance of 21 of these mutations is influenced by NMD. We demonstrate, furthermore, that in the case of myosin, the dominant-negative effects of nonsense alleles are likely to be due to expression of N-terminal nonsense-fragment polypeptides, not to mistranslation of the nonsense codons. mRNA surveillance, therefore, may mitigate potentially deleterious effects of many heterozygous germline and somatic nonsense or frame-shift mutations. We also provide evidence that smg-6, a gene previously identified as being required for NMD, performs essential function(s) in addition to its role in NMD.

Animals↗
PubMed1988

The effects of H-2 and non-H-2 genes on the expulsion of the nematode Trichuris muris from inbred and congenic mice.

Two groups of H-2 congenic strains of mice were compared for their susceptibility to a primary infection with the nematode Trichuris muris. Mice of the BALB genetic background were markedly more resistant than mice of the B10 genetic background, as reflected by the rate of expulsion of T. muris from the large intestine. Within each of the two groups of H-2 congenic strains mice possessing the H-2k haplotype (BALB/k, B10.BR) were more susceptible to infection than mice expressing other haplotypes; B10 background strains expressing H-2b (B10) or H-2q (B10.G) alleles were the most resistant of the four congenic strains studied. Differential resistance was observed within three of the four B10 congenic strains and this is discussed in terms of rate of development of the protective immune response in relation to worm development. The results support the conclusion that both H-2-linked and non-H-2 genes play important roles in controlling the immune response which expels worms from the gut.

Animals↗
PubMed2026

First genomic insights into the introgression of almond PPV-Marcus resistance into peach.

AIM: Sharka, caused by Plum pox virus (PPV), is one of the most damaging viral diseases of stone fruit crops, with peach among the most susceptible cultivated Prunus species. Almond is a promising source of resistance, but its genetic architecture and expression in a peach genetic background remain largely unknown. This study aimed to construct parental genetic linkage maps and identify genomic regions associated with PPV response in almond &#xd7; peach interspecific populations. METHODS: Progenies derived from the almond cultivars 'Del Cid', 'Garrigues', and 'Mono' were evaluated by RT-PCR after graft inoculation with the PPV-Marcus (PPV-M) strain over consecutive infection cycles. Phenotypic data were summarized for each genotype using best linear unbiased estimates (BLUEs). High-density SNP almond and peach arrays were used to construct parental maps for 'Garrigues' and 'Mono' and perform quantitative trait locus (QTL) analysis. RESULTS: Phenotypic variation was observed among and within families. 'Del Cid'-derived progenies showed the greatest resistance, 'Garrigues'-derived progenies displayed intermediate responses, and 'Mono'-derived progenies showed greater susceptibility and variability. The parental maps covered 546.69 cM in 'Mono' and 521.72 cM in 'Garrigues', with average intervals of 0.61 and 1.26 cM per unique marker position, respectively, and showed strong collinearity with the reference genome. QTL associated with PPV-M response were detected on linkage groups (LG) 1 and 6 in 'Garrigues' and LG2 in 'Mono'. The main QTL in 'Garrigues' peaked near 22.39 Mb on LG1, whereas the 'Mono' QTL was located at 22.27-22.62 Mb on LG2; a weaker QTL was detected near 25.38 Mb on LG6 in 'Garrigues'. The results support a quantitative and genetic-background-dependent architecture of PPV resistance. CONCLUSION: This study provides the first evidence of genomic regions associated with PPV-Marcus response in almond &#xd7; peach populations. The detected QTLs provide an initial basis to support the introgression of almond-derived resistance into peach breeding material.

Prunus↗