A new contribution to the integration of human and porcine genome maps: 623 new points of homology

Robic, Annie; Faraut, Thomas; Iannuccelli, Nathalie; Lahbib-Mansais, Y.; Cantegrel, V.; Alexander, L. J.; Milan, Denis

doi:10.1159/000075733

Cited by 18 publications

(17 citation statements)

References 22 publications

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“…These results are in perfect accordance with Robic et al (2003), who reported the corresponding locations of 623 porcine microsatellites on the human genome, comprising those found in this study with the highest LOD scores. These results are in perfect accordance with Robic et al (2003), who reported the corresponding locations of 623 porcine microsatellites on the human genome, comprising those found in this study with the highest LOD scores.…”

Section: Discussionsupporting

confidence: 93%

Analysis and mapping of CACNB4, CHRNA1, KCNJ3, SCN2A and SPG4, physiological candidate genes for porcine congenital progressive ataxia and spastic paresis

Genini

Kratzsch

Korczak

et al. 2007

J Animal Breeding Genetics

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The cause of porcine congenital progressive ataxia and spastic paresis (CPA) is unknown. This severe neuropathy manifests shortly after birth and is lethal. The disease is inherited as a single autosomal recessive allele, designated cpa. In a previous study, we demonstrated close linkage of cpa to microsatellite SW902 on porcine chromosome 3 (SSC3), which corresponds syntenically to human chromosome 2. This latter chromosome contains ion channel genes (Ca(2+), K(+) and Na(+)), a cholinergic receptor gene and the spastin (SPG4) gene, which cause human epilepsy and ataxia when mutated. We mapped porcine CACNB4, KCNJ3, SCN2A and CHRNA1 to SSC15 and SPG4 to SSC3 with the INRA-Minnesota porcine radiation hybrid panel (IMpRH) and we sequenced the entire open reading frames of CACNB4 and SPG4 without finding any differences between healthy and affected piglets. An anti-epileptic drug treatment with ethosuximide did not change the severity of the disease, and pigs with CPA did not exhibit the corticospinal tract axonal degeneration found in humans suffering from hereditary spastic paraplegia, which is associated with mutations in SPG4. For all these reasons, the hypothesis that CACNB4, CHRNA1, KCNJ3, SCN2A or SPG4 are identical with the CPA gene was rejected.

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Section: Discussionsupporting

confidence: 93%

Analysis and mapping of CACNB4, CHRNA1, KCNJ3, SCN2A and SPG4, physiological candidate genes for porcine congenital progressive ataxia and spastic paresis

Genini

Kratzsch

Korczak

et al. 2007

J Animal Breeding Genetics

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“…Second, we shall present the studies aimed at characterizing the metabolic pathways involved and the physiological methodologies used to identify candidate genes. In order to better confront the two approaches, we provide in Table I data on the genes cited in this review with their putative position in the pig genome deduced from their location on the human physical map (http://www.ensembl.org/Homo_sapiens/index.html) and the comparative pig/human map established by Robic et al [34] (http://www2.toulouse.inra.fr/lgc/pig/msat/). Lastly, we shall give some perspectives on the use of these various strategies to identify genes involved in such complex traits.…”

Section: Introductionmentioning

confidence: 99%

“…Updated summary of the data known for the genes cited in this paper. The expected location on the porcine linkage map is deduced from the position in the human genome and the pig/human comparative map proposed by Robic et al [34]. For the CYP2E…”

Section: Introductionmentioning

confidence: 99%

Genetic and metabolic aspects of androstenone and skatole deposition in pig adipose tissue: A review(Open Access publication)

Robic

Larzul²,

Bonneau³

2007

Genet. Sel. Evol.

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-High levels of androstenone and skatole in fat tissues are considered the primary causes of boar taint, an unpleasant odour and flavour of the meat from non-castrated male pigs. The aim of this article is to review our current knowledge of the biology and genetic control of the accumulation of androstenone and skatole in fat tissue. Two QTL mapping studies have shown the complexity of the genetic control of these traits. During the last ten years, several authors have taken a more physiological approach to investigate the involvement of genes controlling the metabolism of androstenone and skatole. Although some authors have claimed the identification of candidate genes, it is more appropriate to talk about target genes. This suggests that genes affecting androstenone and skatole levels will have to be sought for among specific or non-specific transcription factors interacting with these target genes.androstenone / skatole / pig / boar taint / QTL

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“…However, comparative mapping of human and porcine chromosome regions might allow us to postulate some candidate genes that might eventually be responsible for predisposition to AA (see Table 4). The comparative maps established by Goureau et al (1996Goureau et al ( , 2000, Shi et al (2001), and Robic et al (2003) suggest that the region SSC 1q18-q21 flanked by markers SW1621 and SW1902 maps to three different human chromosomal regions: HSA 15q26, HSA 14q22, and HSA 9q21-q34. Our own BLAST searches comparing the porcine flanking sequence of SW1621 and SW1902 to the human genome sequence suggest that it is homologous to HSA 9q34.4.…”

Section: Discussionmentioning

confidence: 99%

“…for genotyping. Olaf Bininda-Emonds, funded by Bundesministerium fü r Bildung und Forschung (Federal Ministery of Education and Research), provided (Goureau et al 1996(Goureau et al , 2000Shi et al 2001;Robic et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Genomewide Scan for Anal Atresia in Swine Identifies Linkage and Association With a Chromosome Region onSus scrofaChromosome 1

2005

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Anal atresia is a rare and severe disorder in swine occurring with an incidence of 0.1-1.0%. A wholegenome scan based on affected half-sibs was performed to identify susceptibility loci for anal atresia. The analysis included 27 families with a total of 95 animals and 65 affected piglets among them. Animals were genotyped for 126 microsatellite markers distributed across the 18 autosomal porcine chromosomes and the X chromosome, covering an estimated 2080 cM. Single-point and multipoint nonparametric linkage scores were calculated using the computer package ALLEGRO 1.0. Significant linkage results were obtained for chromosomes 1, 3, and 12. Markers on these chromosomes and additionally on chromosomes for which candidate genes have been postulated in previous studies were subjected to the transmission disequilibrium test (TDT). The test statistic exceeded the genomewide significance level for adjacent markers SW1621 (P ¼ 7 3 10 ÿ7 ) and SW1902 (P ¼ 3 3 10 ÿ3 ) on chromosome 1, supporting the results of the linkage analysis. A specific haplotype associated with anal atresia that could prove useful for selection against the disorder was revealed. Suggestive linkage and association were also found for markers S0081 on chromosome 9 and SW957 on chromosome 12.

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A new contribution to the integration of human and porcine genome maps: 623 new points of homology

Cited by 18 publications

References 22 publications

Analysis and mapping of CACNB4, CHRNA1, KCNJ3, SCN2A and SPG4, physiological candidate genes for porcine congenital progressive ataxia and spastic paresis

Analysis and mapping of CACNB4, CHRNA1, KCNJ3, SCN2A and SPG4, physiological candidate genes for porcine congenital progressive ataxia and spastic paresis

Genetic and metabolic aspects of androstenone and skatole deposition in pig adipose tissue: A review(Open Access publication)

Genomewide Scan for Anal Atresia in Swine Identifies Linkage and Association With a Chromosome Region onSus scrofaChromosome 1

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