Localization on pig chromosome 6 of markers GPI, APOE, and ENO1, carried by human chromosomes 1 and 19, using in situ hybridization

Yerle, Martine M.; Gellin, Joël; Dalens, M.; Galman, O

doi:10.1159/000132966

Cited by 26 publications

(11 citation statements)

References 4 publications

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“…Intriguingly, the close linkage of FH-r and INSR on SSC2 together with the fact that INSR is on HSA19 near the human LDLR locus presented LDLR as the prime candidate gene for FH-r in pigs. At the same time the genes for apolipoproteins; (APO)B (SSC3) [Solinas et al, 1992], A1, C3 and R (SSC9) [Ellegren, 1994;Cepica et al, 1996;Hasler-Rapacz et al, unpublished], and APOE (SSC6) [Yerle et al, 1990], as well as one encoding a key lipid enzyme; LPL (SSC14) [Gu et al, 1992], could be excluded as candidate genes for FH-r since they reside on other pig chromosomes.…”

Section: Identification Of the Ldlr As A Candidate Gene By Comparativmentioning

confidence: 99%

Identification of a mutation in the low density lipoprotein receptor gene associated with recessive familial hypercholesterolemia in swine

et al. 1998

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Elevated blood plasma cholesterol (hypercholesterolemia) is a major risk factor for coronary artery disease (CAD) in humans. Genetic dissection of polygenic lipid and lipoprotein disorders in swine, a key animal model for the study of familial hypercholesterolemia (FH) and CAD, led to the isolation of a monogenic subphenotype (FH-r), that is inherited in the recessive (r) manner. A genome scan mapped the FH-r locus close to the centromere of chromosome 2. Comparative mapping showed that this region shares homology with a part of human chromosome 19 that harbors the low density lipoprotein receptor (LDLR) locus, and therefore suggested LDLR as the prime candidate gene for FH-r. Cloning and sequencing of hepatic LDLR cDNA from two FH-r/r and one normal (N/N) animals disclosed a single missense mutation (R84C) in a region that corresponds to human exon 4. The C84 mutation cosegregates invariantly with hypercholesterolemia, which strongly suggests that this mutation is responsible for the observed hyperlipidemia.

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Section: Identification Of the Ldlr As A Candidate Gene By Comparativmentioning

confidence: 99%

Identification of a mutation in the low density lipoprotein receptor gene associated with recessive familial hypercholesterolemia in swine

et al. 1998

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“…In humans, the ryanodine receptor gene has been mapped to the q13.1 region of the chromosome 19 (McKenzie et al 1990) and is very close to genetic markers, GPI. TGFPl (transforming growth factor PI) and APOE (apolipprotein E), which have been shown to be tightly linked to the malignant hyperthermia locus in humans (McCarthy et al 1990) as well as to the halothane sensitivity locus in pigs (Chowdhary et al 1989;Yerle et al 1990aYerle et al , 1990b. The linkage study carried out by McLennan e f al.…”

Section: Genetic Markersmentioning

confidence: 99%

Genetics of Pig Meat Quality: A Review

Sellier

Monin²

1994

Journal of Muscle Foods

130

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This paper is a review of current knowledge about genetic effects on technological and eating qualities of pork. These effects have been recognized as primordial sources of variation of meat quality in the porcine species. Nevertheless, some significant advances have recently been obtained in this area. This literature survey reveals that: The halothane sensitivity gene (HALn) explains to a large extent the overall genetic variation in technological quality and eating quality of pork. Evidence is accumulating that the halothane sensitivity gene is not completely recessive regarding its effects on quality traits. Producing slaughter pigs heterozygous at the HAL locus may result in deficiencies in meat quality, probably depending on slaughter conditions and perhaps also on slaughter weight. Breed differences in technological and sensory qualities of pork partly result from the large breed variation in incidence of halothane sensitivity, but other factors are implied, particularly ultimate pH and intramuscular fat content of meat. The major dominant gene RN‐is probably at the origin of the previously described “Hampshire effect” on meat quality. Heritability of most traits referring to the technological quality of meat is low to moderate (0.15 to 0.30), whereas heritability of intramuscular fat content is high (0.40 to 0.50). A genetic antagonism exists between technological quality of pork and growth or body composition traits. The halothane sensitivity gene is the major factor responsible for the “meat quantity — meat quality” genetic antagonism.

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“…Fluorescent in situ hybridization (FISH) was performed to determined the chromosomal location of the porcine apo-E gene. Using a radioactively labelled human probe, Yerle et al (1990) had tentatively assigned the apo-E gene to chromosome 6 band q2z1 by in situ hybridization. The FISH procedure followed standard protocols (Pinkel et al 1986) with slight modifications as previously described (Gallagher et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Isolation and genetic characterization of the porcine apolipoprotein E gene

et al. 1998

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The present report describes the isolation and genetic characterization of the porcine apolipoprotein E (apo-E) gene. A single positive recombinant phage clone containing a 10.7-kb insert was isolated from a porcine genomic library, and a 4.2-kb fragment was subcloned and sequenced. The 4.2-kb fragment contained the entire apo-E gene in addition to upstream and downstream sequences (GenBank accession no. 470240). The porcine apo-E gene is made up of four exons and three introns, and encodes a preapo-E protein comprised of a signal peptide of 18 amino acids and a mature protein of 299 amino acids. The porcine apo-E gene contains a (CG)13 microsatellite marker within intron three. This microsatellite is moderately polymorphic, and at least four alleles were evident at this locus among 10 animals from each of the Yorkshire, Hampshire, Landrace and Duroc breeds. Finally, localization of the porcine apo-E gene to chromosome 6 band q2.1 was determined by fluorescent in situ hybridization and confirmed by genetic linkage analysis.

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Localization on pig chromosome 6 of markers GPI, APOE, and ENO1, carried by human chromosomes 1 and 19, using in situ hybridization

Cited by 26 publications

References 4 publications

Identification of a mutation in the low density lipoprotein receptor gene associated with recessive familial hypercholesterolemia in swine

Identification of a mutation in the low density lipoprotein receptor gene associated with recessive familial hypercholesterolemia in swine

Genetics of Pig Meat Quality: A Review

Isolation and genetic characterization of the porcine apolipoprotein E gene

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