scholarly journals TRAITS THAT INFLUENCE LONGEVITY IN MICE

Genetics ◽  
1984 ◽  
Vol 108 (4) ◽  
pp. 999-1011
Author(s):  
Edmond J Yunis ◽  
Ada L M Watson ◽  
Rebecca S Gelman ◽  
Sherrill J Sylvia ◽  
Roderick Bronson ◽  
...  
Keyword(s):  
Life Span ◽  
Causes Of Death ◽  
Coat Color ◽  
Genetic Interactions ◽  
Chromosome 9 ◽  
Chromosome 17 ◽  
Chromosome 4 ◽  
Limited Extent ◽  
Month Of Birth ◽  
Genetic And Environmental Factors

ABSTRACT Analysis of genetic interactions in the segregating backcross [(C57BL/6 x DBA/2)F1 x DBA/2] mice revealed influences of genetic and environmental factors on life span. Using determinants of coat color (brown locus of chromosome 4 and dilute locus of chromosome 9), serologically determined H-2 antigens (chromosome 17) and sex as genetic markers, we studied the effects of these genes on longevity. The results suggested that genes in the brown locus (b) segment of chromosome 4, genes in a segment of the sex chromosomes and, to a more limited extent, genes in the segment of chromosome 17 which contains the H-2 haplotype all influenced longevity. The coat color (b locus) segment of chromosome 4 was associated with life span predominantly in females, whereas the chromosome 17 (H-2 haplotype) segment was associated with longer life primarily in males. The dilute locus d segment on chromosome 9 did not affect life span. Longevity appears to be influenced by interactions between genes in the chromosomal segment carrying H-2, those in the b segment, gender and the month of birth. Greater heterozygosity at the loci studied was associated with longer life span. Histopathological findings on mice that died at or after 28 months of age were comparable for all genetic combinations except that there was an increased frequency of lymphoma in females and an increased frequency of amyloidosis in males. Our analysis emphasizes the need for comprehensive studies of aging and longevity that would simultaneously determine the effects of several genetic regions and their interactions with the environment with respect to possible causes of death.

scholarly journals Traits that influence longevity in mice: a second look.

Genetics ◽  
1992 ◽  
Vol 132 (1) ◽  
pp. 229-239
Author(s):  
K B Dear ◽  
M Salazar ◽  
A L Watson ◽  
R S Gelman ◽  
R Bronson ◽  
...  
Keyword(s):  
Life Span ◽  
Genetic Factors ◽  
Viral Infections ◽  
Genetic Interactions ◽  
Chromosome 9 ◽  
Chromosome 4 ◽  
Histological Findings ◽  
Male And Female ◽  
Female Genotype ◽  
Dominant Black

Abstract Analysis of genetic interactions in the F2 of an intercross of (C57BL/6 x DBA/2) F1J revealed influences of genetic factors on life span. Females lived longer than males. Dilute brown females died sooner than females of other colors. H-2b/H-2b males died sooner than H-2b/H-2d or H-2d/H-2d males, except that among dilute brown males those of typeH-2b/H-2d died sooner. Cluster analysis suggested that male and female genotypes each fall into two groups, with female dilute brown mice having shorter lives than other females, and male H-2b/H-2b mice except dilute brown and dilute brown H-2b/H-2d mice having shorter lives than other males. The association of heterozygosity with life span was clearer in females than in males, yet the longest-lived female genotype was homozygous H-2d/H-2d, of dominant Black phenotype at the Brown locus of chromosome 4, and homozygous dd at the Dilute locus of chromosome 9. The shortest-lived females were dilute brown H-2b/H-2b. The longest-lived and shortest-lived male genotypes were dilute brown H-2d/H-2d and dilute brown H-2b/H-2d, respectively. Although histological findings at postmortem differed between the sexes, there was no association of particular disorders with other genetic markers. The importance of H-2 in males was confirmed, but the allelic effects were perturbed, possibly by the absence of Sendai infection in this experiment. Overall our studies suggest that genetic influences on life span involve interactions between loci, and allelic interactions may change with viral infections or other environmental factors.

scholarly journals Factors affecting the observed number of young resulting from adjacent-2 disjunction in mice carrying a translocation

1977 ◽  
Vol 29 (1) ◽  
pp. 83-92 ◽  
Author(s):  
Mary F. Lyon ◽  
P. H. Glenister
Keyword(s):  
Reciprocal Translocation ◽  
Proximal Region ◽  
Chromosome 9 ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Marker Genes ◽  
Factors Affecting ◽  
Male Gametes

SUMMARYThe frequency of adjacent-2 disjunction in mice carrying the reciprocal translocation T(9; 17)138Ca was studied by mating together animals heterozygous for the translocation and carrying different recessive marker genes, using Tt for chromosome 17 and cwcw for chromosome 9. The proportion of marked young arising from adjacent-2 disjunction varied according to the markers carried in the two parents. When the female carried Tt the frequencies of marked young were always higher than when non-T females were used, and when Tt and cwcw were carried in the same parent there was a shortage of marked young obtaining both copies of the proximal region of chromosome 17 from the father. Both these effects were regarded as probably another example of the phenomenon discovered by Johnson, of inviability of young lacking a maternal homologue of a certain region of chromosome 17. There were other variations in frequency of marked young, among crosses using non-T females, which may have been due to differences in transmission ratio of male gametes carrying various t-haplotypes or to true variations in frequency of adjacent-2 disjunction.

CHROMOSOME BANDING HOMOLOGIES OF A TANDEM FUSION IN RIVER, SWAMP, AND CROSSBRED BUFFALOES (BUBALUS BUBALIS)

1982 ◽  
Vol 24 (6) ◽  
pp. 667-673 ◽  
Author(s):  
T. A. Bongso ◽  
M. Hilmi
Keyword(s):  
First Generation ◽  
Bubalus Bubalis ◽  
Chromosome 9 ◽  
Chromosome 4 ◽  
Centromere Region ◽  
Hybrid Female ◽  
Banding Patterns ◽  
C Banding ◽  
Tandem Fusion ◽  
Y Chromosomes

The chromosomes of the Murrah (River), Swamp (Malaysian kerbau), F1 hybrid (Murrah × Swamp) and first generation backcross (F1 hybrid female × Murrah male) buffaloes (Bubalus bubalis L.) were studied using Giemsa (G) and centromeric (C) banding techniques. The diploid chromosome number for the Murrah was 2n = 50, Swamp 2n = 48, F1 hybrid 2n = 49 and two backcross animals had 2n = 49 and 2n = 50, respectively. The largest two metacentric chromosomes of the Swamp resulted from a tandem fusion between the two chromosomes 4p and 9, respectively, of the Murrah karyotype. The F1 hybrid (2n = 49) and one of the backcrosses (2n = 49) had karyotypes intermediate to the Murrah and Swamp parents. The C banding patterns were useful in identifying the X and Y chromosomes of the buffalo and demonstrated that a major portion of the centromere region of chromosome 9 was not incorporated into chromosome 4 during the tandem fusion.

scholarly journals Resistance to Leishmania major is Linked to the H2 Region on Chromosome 17 and to Chromosome 9

1997 ◽  
Vol 185 (9) ◽  
pp. 1705-1710 ◽  
Author(s):  
Lynden J. Roberts ◽  
Tracey M. Baldwin ◽  
Joan M. Curtis ◽  
Emanuela Handman ◽  
Simon J. Foote
Keyword(s):  
Leishmania Major ◽  
Systemic Disease ◽  
Continuous Distribution ◽  
Clinical Manifestations ◽  
Chromosome 9 ◽  
Chromosome 17 ◽  
Self Healing ◽  
Genome Wide ◽  
A Genome ◽  
Murine Cutaneous Leishmaniasis

In Leishmaniasis, as in many infectious diseases, clinical manifestations are determined by the interaction between the genetics of the host and of the parasite. Here we describe studies mapping two loci controlling resistance to murine cutaneous leishmaniasis. Mice infected with L. major show marked genetic differences in disease manifestations: BALB/c mice are susceptible, exhibiting enlarging lesions that progress to systemic disease and death, whereas C57BL/6 are resistant, developing small, self-healing lesions. F2 animals from a C57BL/6 × BALB/c cross showed a continuous distribution of lesion score. Quantitative trait loci (QTL) have been mapped after a non-parametric QTL analysis on a genome-wide scan on 199 animals. QTLs identified were confirmed in a second cross of 271 animals. Linkage was confirmed to a chromosome 9 locus (D9Mit67–D9Mit71) and to a region including the H2 locus on chromosome 17. These have been named lmr2 and lmr1, respectively.

scholarly journals Genetic evidence for two t complex tail interaction (tct) loci in t haplotypes.

Genetics ◽  
1989 ◽  
Vol 122 (4) ◽  
pp. 895-903
Author(s):  
J H Nadeau ◽  
D Varnum ◽  
D Burkart
Keyword(s):  
Genetic Analysis ◽  
Tail Length ◽  
Genetic Interactions ◽  
Chromosome 17 ◽  
Wild Type ◽  
T Complex ◽  
Inverted Duplication ◽  
Haplotype A ◽  
Recombination Breakpoints ◽  
T Haplotype

Abstract The t complex on chromosome 17 of the house mouse is an exceptional model for studying the genetic control of transmission ratio, gametogenesis, and embryogenesis. Partial haplotypes derived through rare recombination between a t haplotype and its wild-type homolog have been essential in the genetic analysis of these various properties of the t complex. A new partial t haplotype, which was derived from the complete tw71 haplotype and which is called tw71Jr1, was shown to have unexpected effects on tail length and unique recombination breakpoints. This haplotype, either when homozygous or when heterozygous with the progenitor tw71 haplotype, produced short-tailed rather than normal-tailed mice on certain genetic backgrounds. Genetic analysis of this exceptional haplotype showed that the recombination breakpoints were different from those leading to any other partial t haplotype. Based on this haplotype, a model is proposed that accounts for genetic interactions between the brachyury locus (T), the t complex tail interaction (tct) locus, and their wild-type homolog(s) that determine tail length. An important part of this model is the hypothesis that the tct locus, which enhances the tail-shortening effect of T mutations, is in fact at least two, genetically separable genes with different genetic activities. Genetic analysis of parental and recombinant haplotypes also suggests that intrachromosomal recombination involving an inverted duplicated segment can account for the variable orientation of loci within an inverted duplication on wild-type homologs of the t haplotype.

scholarly journals Partial trisomy 4q and monosomy 5p inherited from a maternal translocationt(4;5)(q33;p15) in three adverse pregnancies

2020 ◽  
Author(s):  
Jingbo Zhang ◽  
Bei Zhang ◽  
Tong Liu ◽  
Huihui Xie ◽  
Jingfang Zhai
Keyword(s):  
Prenatal Diagnosis ◽  
Chromosomal Abnormalities ◽  
Genetic Diagnosis ◽  
Partial Trisomy ◽  
Distal Region ◽  
Chromosome 17 ◽  
Chromosome 1 ◽  
Chromosome 4 ◽  
Chromosome 5 ◽  
Balanced Translocation

Abstract Background: Carriers of balanced reciprocal chromosomal translocations are at known reproductive risk for offspring with unbalanced genotypes and resultantly abnormal phenotypes. Once fertilization of a balanced translocation gamete with a normal gamete, the partial monomer or partial trisomy embryo will undergo abortion, fetal arrest or fetal malformations. We reported a woman with chromosomal balanced translocation who had two adverse pregnancies. Prenatal diagnosis was made for her third pregnancy to provide genetic counseling and guide her fertility. Case presentation: We presented a woman with chromosomal balanced translocation who had three adverse pregnancies. Routine G banding and CNV-seq were used to analyze the chromosome karyotypes and copy number variants of amniotic fluid cells and peripheral blood. The karyotype of the woman was 46,XX,t(4;5)(q33;p15). During her first pregnancy, odinopoeia was performed due to fetal edema and abdominal fluid. The umbilical cord tissue of the fetus was examined by CNV-seq. The results showed a genomic gain of 24.18 Mb at 4q32.3-q35.2 and a genomic deletion of 10.84 Mb at 5p15.33-p15.2 and 2.36 Mb at 15q11.1-q11.2. During her second pregnancy, she did not receive a prenatal diagnosis because a routine prenatal ultrasound examination found no abnormalities. In 2016, she gave birth to a boy.. The karyotype the of the boy was 46,XY,der(5)t(4;5)(q33;p15)mat. The results of CNV-seq showed a deletion of short arm of chromosome 5 capturing regions 5p15.33p15.2, a copy gain of the distal region of chromosome 4 at segment 4q32.3q35.2, a duplication of chromosome 1 at segment 1q41q42.11 and a duplication of chromosome 17 at segment 17p12. During her third pregnancy, she underwent amniocentesis at 17 weeks of gestation. Chromosome karyotype hinted 46,XY,der(5)t(4;5)(q33;p15)mat. Results of CNV-seq showed a deletion of short arm (p) of chromosome 5 at the segment 5p15.33p15.2 and a duplication of the distal region of chromosome 4 at segment 4q32.3q35.2.Conclusions: Chromosomal abnormalities in three pregnancies were inherited from the mother. Preimplantation genetic diagnosis is recommended to prevent the birth of children with chromosomal abnormalities.

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