14,194 research outputs found

    Forced Running Endurance Is Influenced by Gene(s) on Mouse Chromosome 10

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    Acknowledgments The authors wish to acknowledge technical assistance from Mrs. Indr臈 Libnickien臈 and intellectual input from Dr. David A. Blizard. This research was funded by the European Social Fund under the Global Grant measure. Grant VP1-3.1-艩MM-07-K-02-057 was awarded to AL.Peer reviewedPublisher PD

    Loss of chromosome 10 is an independent prognostic factor in high-grade gliomas

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    Loss of heterozygosity (LOH) for chromosome 10 is the most frequent genetic abnormality observed in high-grade gliomas. We have used fluorescent microsatellite markers to examine a series of 83 patients, 34 with anaplastic astrocytoma (grade 3) and 49 with glioblastoma multiforme (grade 4), for LOH of chromosome 10. Genotype analysis revealed LOH for all informative chromosome 10 markers in 12 (35%) of patients with grade 3 and 29 (59%) grade 4 tumours respectively, while partial LOH was found in a further eight (24%) grade 3 and ten (20%) grade 4 tumours. Partial LOH, was confined to the long arm (10q) in six and the short arm (10p) in three cases, while alleles from both arms were lost in four cases. Five tumours (one grade 3 and four grade 4) showed heterogeneity with respect to loss at different loci. There was a correlation between any chromosome 10 loss and poorer performance status at presentation (蠂2P = 0.005) and with increasing age at diagnosis (Mann鈥揥hitney U-test P = 0.034) but not with tumour grade (蠂2P = 0.051). A Cox multivariate model for survival duration identified age (proportional hazards (PH), P = 0.004), grade (PH, P = 0.012) and any loss of chromosome 10 (PH, P = 0.009) as the only independent prognostic variables. Specifically, LOH for chromosome 10 was able to identify a subgroup of patients with grade 3 tumours who had a significantly shorter survival time. We conclude that LOH for chromosome 10 is an independent, adverse prognostic variable in high-grade glioma. 漏 1999 Cancer Research Campaig

    Chromosome 10 in the tomato plant carries clusters of genes responsible for field resistance/defence to Phytophthora infestans

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    AbstractThe main objective of the present study was to reanalyse tomato expression data that was previously submitted to the Tomato Expression Database to dissect the resistance/defence genomic and metabolic responses of tomato to Phytophthora infestans under field conditions. Overrepresented gene sets belonging to chromosome 10 were identified using the Gene Set Enrichment Analysis, and we found that these genes tend to be located towards the end of the chromosome 10. An analysis of syntenic regions between Arabidopsis thaliana chromosomes and the tomato chromosome 10 allowed us to identify conserved regions in the two genomes. In addition to allowing for the identification of tomato candidate genes participating in resistance/defence in the field, this approach allowed us to investigate the relationships of the candidate genes with chromosomal position and participation in metabolic functions, thus offering more insight into the phenomena occurring during the infection process

    Mouse chromosome 10

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47005/1/335_2004_Article_BF00360836.pd

    ReAS: Recovery of Ancestral Sequences for Transposable Elements from the Unassembled Reads of a Whole Genome Shotgun

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    We describe an algorithm, ReAS, to recover ancestral sequences for transposable elements (TEs) from the unassembled reads of a whole genome shotgun. The main assumptions are that these TEs must exist at high copy numbers across the genome and must not be so old that they are no longer recognizable in comparison to their ancestral sequences. Tested on the japonica rice genome, ReAS was able to reconstruct all of the high copy sequences in the Repbase repository of known TEs, and increase the effectiveness of RepeatMasker in identifying TEs from genome sequences

    The gene order on Human Chromosome 15 and Chicken Chromosome 10 reveal multiple inter- and intrachromosomal rearrangements

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    Comparative mapping between the human and chicken genomes has revealed a striking conservation of synteny between the genomes of these two species, but the results have been based on low-resolution comparative maps. To address this conserved synteny in much more detail, a high-resolution human-chicken comparative map was constructed from human chromosome 15. Mapping, sequencing, and ordering of specific chicken bacterial artificial chromosomes has improved the comparative map of chromosome 15 (Hsa15) and the homologous regions in chicken with almost 100 new genes and/or expressed sequence tags. A comparison of Hsa15 with chicken identified seven conserved chromosomal segments between the two species. In chicken, these were on chromosome 1 (Gga1; two segments), Gga5 (two segments), and Gga10 (three segments). Although four conserved segments were also observed between Hsa15 and mouse, only one of the underlying rearrangement breakpoints was located at the same position as in chicken, indicating that the rearrangements generating the other three breakpoints occurred after the divergence of the rodent and the primate lineages. A high-resolution comparison of Gga10 with Hsa15 identified 19 conserved blocks, indicating the presence of at least 16 intrachromosomal rearrangement breakpoints in the bird lineage after the separation of birds and mammals. These results improve our knowledge of the evolution and dynamics of the vertebrate genomes and will aid in the clarification of the mechanisms that underlie the differentiation between the vertebrate species

    Mapping quantitative trait loci for seizure response to a GABAA receptor inverse agonist in mice

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    To define the genetic contributions affecting individual differences in seizure threshold, a beta carboline [methyl-beta-carboline-3-carboxylate (beta-CCM)]-induced model of generalized seizures was genetically dissected in mice. beta-CCM is a GABAA receptor inverse agonist and convulsant. By measuring the latency to generalized seizures after beta-CCM administration to A/J and C57BL6/J mice and their progeny, we estimated a heritability of 0.28 +/- 0.10. A genome wide screen in an F2 population of these parental strains (n = 273) mapped quantitative trait loci (QTLs) on proximal chromosome 7 [logarithm of the likelihood for linkage (LOD) = 3.71] and distal chromosome 10 (LOD = 4.29) for seizure susceptibility, explaining approximately 22 and 25%, respectively, of the genetic variance for this seizure trait. The best fitting logistic regression model suggests that the A/J allele at each locus increases the likelihood of seizures approximately threefold. In a subsequent backcross population (n = 223), we mapped QTLs on distal chromosome 4 (LOD = 2.88) and confirmed the distal chromosome 10 QTLs (LOD = 4.36). In the backcross, the C57BL/6J allele of the chromosome 10 QTL decreases the risk of seizures approximately twofold. These QTLs may ultimately lead to the identification of genes influencing individual differences in seizure threshold in mice and the discovery of novel anticonvulsant agents. The colocalization on distal chromosome 10 of a beta-CCM susceptibility QTL and a QTL for open field ambulation and vertical movement suggests the existence of a single, pleiotropic locus, which we have named Exq1