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The human apolipoprotein B-100 gene: a highly polymorphic gene that maps to the short arm of chromosome 2.

Using a cloned cDNA of apolipoprotein B-100 as hydridization probe, we have found high frequence polymorphisms in the apoB-100 gene involving sites for the restriction enzymes EcoRI, BamHI, and HindIII. The major EcoRI polymorphisms involved a 17 kb vs 15 kb variant. The incidence of the various phenotypes was estimated. In addition, other complex polymorphisms involving MspI and TaqI sites were also noted. [32P]-labeled apoB-100 cDNA was used as a probe in chromosome mapping studies to detect the human apoB-100 structural gene sequence in human-Chinese hamster and human-mouse cell hybrids. Southern blot analysis of 14 hybrids localized the gene to the short arm of human chromosome 2.

Apolipoprotein B-100↗

Deletion map of chromosome 9 and p16 (CDKN2A) gene alterations in neuroblastoma.

We reported previously that loss of heterozygosity (LOH) on chromosomes 2q, 9p and 18q frequently occurs in neuroblastoma and that patients with 9p LOH in the tumors showed statistically significant association with an advanced stage of the disease and poor prognosis. To determine the role of chromosome 9 loss in neuroblastoma, we performed deletion mapping of chromosome 9 in 80 cases of neuroblastoma using 11 polymorphic microsatellite markers and a restriction fragment length porymorphism marker. LOH at one or more loci on chromosome 9 was detected in 33 of 80 cases (41%). Chromosome 9p was lost in 24 of 80 cases (32%), whereas chromosome 9q was lost in 18 of 80 cases (23%). There were two commonly deleted regions mapped to 9p21 between the D9S171 marker and the IFNB1 marker and 9q34-qter distal to the D9S176 marker. In addition, patients with LOH at 9p21 but not at 9q34-qter in the tumors showed statistically significant association with poor prognosis (P = 0.023). Because the commonly deleted regions at 9p21 includes the p16 (CDKN2A) gene, the status of the p16 gene was further examined in 80 fresh tumors and 19 cell lines of neuroblastoma. A missense mutation was detected at codon 52 in a fresh tumor. The p16 gene was not expressed in 13 of 19 cell lines (72%), and 5 of the 13 cell lines displayed methylation of the CpG island surrounding the first exon of the p16 gene. These results suggest that the p16 gene is a candidate tumor suppressor gene for neuroblastoma, and its inactivation may contribute to the progression of neuroblastoma.

Carrier Proteins↗

A physical and genetic map of the Mycoplasma flocculare ATCC 27716 chromosome reveals large genomic inversions when compared with that of Mycoplasma hyopneumoniae strain J(T).

Pulsed-field gel electrophoresis and DNA hybridization data were used to construct a chromosomal map of Mycoplasma flocculare ATCC 27716, a non-pathogenic inhabitant of porcine respiratory tracts. Twenty-one genetic markers were placed on the map. Comparison of the genetic map with that of the closely related Mycoplasma hyopneumoniae strain J(T), the type strain of the causative agent of enzootic pneumonia in pigs, identified three chromosomal inversions that differentiate these genomes. One of these inversions involves genes that possibly may be involved in M. hyopneumoniae pathogenicity.

Animals↗

A high-density physical map of Sinorhizobium meliloti 1021 chromosome derived from bacterial artificial chromosome library.

As part of the European Sinorhizobium meliloti (strain 1021) chromosome sequencing project, four genomic bacterial artificial chromosome (BAC) libraries have been constructed, one of which was mainly used for chromosome mapping. This library consists of 1,824 clones with an average insert size of 80 kilobases and represents approximately 20-fold total genome coverage [6.8 megabases (Mbs)]. PCR screening of 384 BAC clones with 447 chromosomal markers (PCR primer pairs), consisting of 73 markers representing 118 genes (40 individual genes and 78 genes clustered in 23 operons), two markers from the rrn operon (three loci), four markers from insertion sequences (approximately 16 loci) and 368 sequence-tagged sites allowed the identification of 252 chromosomal BAC clones and the construction of a high-density physical map of the whole 3.7-Mb chromosome of S. meliloti. An average of 5.5 overlapping and colinear BAC clones per marker, correlated with a low rate of deleted or rearranged clones (0.8%) indicate a solid BAC contigation and a correct mapping. Systematic BLASTX analysis of sequence-tagged site marker sequences allowed prediction of a biological function for a number of putative ORFs. Results are available at. This map, whose resolution averages one marker every 9 kilobases, should provide a valuable tool for further sequencing, functional analysis, and positional cloning.

Chromosome Mapping↗

Identification of human OGR1, a novel G protein-coupled receptor that maps to chromosome 14.

We describe the cloning of a novel G protein-coupled receptor, termed ovarian cancer G protein-coupled receptor 1 (OGR1), from an ovarian cancer cell line that maps to chromosome 14q31. The predicted open reading frame of OGR1 encodes a protein of 365 amino acids. OGR1 is expressed as a single 3.0-kb transcript in several tissues, including spleen, testis, small intestine, peripheral blood leukocytes, brain, heart, lung, placenta, and kidney, with no detectable OGR1 expression in thymus, prostate, ovary, colon, liver, skeletal muscle, or pancreas. OGR1 shares strongest homology (49-54%) with the human orphan receptor GPR4. The structural features of OGR1 suggest that the ligand for OGR1 is likely to be a small peptide or a small bioactive molecule.

Amino Acid Sequence↗

Identification of human candidate genes for male infertility by digital differential display.

Evidence for the importance of genetic factors in male fertility is accumulating. In the literature and the Mendelian Cytogenetics Network database, 265 cases of infertile males with balanced reciprocal translocations have been described. The candidacy for infertility of 14 testis-expressed transcripts (TETs) were examined by comparing their chromosomal mapping position to the position of balanced reciprocal translocation breakpoints found in the 265 infertile males. The 14 TETs were selected by using digital differential display (electronic subtraction) to search for apparently testis-specific transcripts in the TIGR database. The testis specificity of the 14 TETs was further examined by reverse transcription-polymerase chain reaction (RT-PCR) on adult and fetal tissues showing that four TETs (TET1 to TET4) were testis-expressed only, six TETs (TET5 to TET10) appeared to be differentially expressed and the remaining four TETs (TET11 to TET14) were ubiquitously expressed. Interestingly, the two tesis expressed-only transcripts, TET1 and TET2, mapped to chromosomal regions where seven and six translocation breakpoints have been reported in infertile males respectively. Furthermore, one ubiquitously, but predominantly testis-expressed, transcript, TET11, mapped to 1p32-33, where 13 translocation breakpoints have been found in infertile males. Interestingly, the mouse mutation, skeletal fusions with sterility, sks, maps to the syntenic region in the mouse genome. Another transcript, TET7, was the human homologue of rat Tpx-1, which functions in the specific interaction of spermatogenic cells with Sertoli cells. TPX-1 maps to 6p21 where three cases of chromosomal breakpoints in infertile males have been reported. Finally, TET8 was a novel transcript which in the fetal stage is testis-specific, but in the adult is expressed in multiple tissues, including testis. We named this novel transcript fetal and adult testis-expressed transcript (FATE).

Chromosome Mapping↗

A novel autosomal recessive nonsyndromic hearing impairment locus (DFNB42) maps to chromosome 3q13.31-q22.3.

A consanguineous family with autosomal recessive nonsyndromic hearing impairment (NSHI) was ascertained in Pakistan and displayed significant evidence of linkage to 3q13.31-q22.3. The novel locus (DFNB42) segregating in this kindred, maps to a 21.6 cM region according to a genetic map constructed using data from both the deCode and Marshfield genetic maps. This region of homozygosity is flanked by markers D3S1278 and D3S2453. A maximum multipoint LOD score of 3.72 was obtained at marker D3S4523. DFNB42 represents the third autosomal recessive NSHI locus to map to chromosome 3.

Audiometry↗

Loss of heterozygosity for DNA polymorphisms mapping to chromosomes 10 and 17 and prognosis in patients with gliomas.

Twenty nine patients with gliomas were investigated for loss of heterozygosity for 40 DNA polymorphisms in tumour DNA, particularly concentrating on those mapping to chromosomes 10 and 17. Eight of 18 grade IV gliomas showed loss of sequences from chromosomes 10, 17, or both. The data suggested total loss of one copy of chromosome 10, but there were interstitial deletions of the short arm of chromosome 17 in three of five tumours. Heterogeneous interstitial deletions of chromosome 17 were also found in two lower grade astrocytomas and one benign oligodendroglioma. The striking finding of this study was that patients with high grade gliomas whose tumours exhibited loss of heterozygosity for chromosomes 10, 17, or both survived significantly longer after surgery (median 17.4 months) than those whose tumours did not show loss of these chromosomes (median 6.7 months). These findings suggest that there is a subset of particularly aggressive high grade gliomas with no currently known molecular genetic abnormalities.

Adult↗

Tumor deletion mapping of chromosomal region 13q14 in 43 growth hormone secreting pituitary adenomas.

Previous studies have reported allelic loss in chromosomal region 13q14 in pituitary tumors. However, the role of RB1 in this region has not been clarified. We performed a tumor deletion map of chromosomal region 13q14 with pituitary adenomas and matched blood samples of 43 patients with acromegaly. Twenty-one patients had non-invasive tumors, 19 had invasive tumors, and in 3 this information was not available. Results showed loss of heterozygosity in at least one microsatelite marker of region 13q14 in 12% (5 of 43) of the somatotropinomas. Retention of marker D13S1325, telomeric to RB1, suggests that the putative tumor suppressor gene is located centromeric to this region, which includes RB1 locus. The participation of RB1 was excluded in four of the five cases because retinoblastoma protein was shown to be positive in these tumors in our previous study. Allelic loss occurred in similar frequency in invasive and noninvasive adenomas. In summary, we confirmed the participation of chromosomal region 13q14 in a subset of GH-secreting adenomas with no regard to tumor grade. RB1 was not implicated, suggesting the participation of another tumor suppressor gene in this region during the first steps of somatotropinoma development.

Acromegaly↗

A complex bilateral polysyndactyly disease locus maps to chromosome 7q36.

We demonstrated that the gene responsible for a congenital limb deformity (polysyndactyly) maps to chromosome 7q36 in a large family. Pre- and postaxial anomalies of the extremities are inherited in this family as an autosomal dominant trait. The disease locus is closely linked to D7S550 (maximum lod score = 6.85, theta = 0). This region is homologous to a segment of mouse chromosome 5, where the mutations hammer toe (HM) and hemimelic extra toes (HX) have been mapped. These data suggest that human chromosome 7q36 and the homologous region of mouse chromosome 5 contain genes involved in limb pattern formation.

Base Sequence↗

Cloning of the human genomic amiloride-sensitive Na+/H+ antiporter gene, identification of genetic polymorphisms, and localization on the genetic map of chromosome 1p.

We have cloned and mapped a 90-kb region spanning the human genomic amiloride-sensitive Na+/H+ antiporter gene on overlapping cosmid clones. This cloned region extends 27 kb upstream of the 5' end of the longest antiporter cDNA and reveals a primary transcription unit of at least 60 kb. Using these genomic clones we have identified polymorphisms in the antiporter gene in human genomic DNA cleaved with enzymes TaqI and MspI; both are two-allele systems. We have localized both polymorphisms to the same segment within an intron of the antiporter transcription unit. Observed heterozygosity for both markers is 47% in 175 unrelated individuals, with the two polymorphic systems showing complete linkage disequilibrium. We have determined genotypes at the antiporter locus in 667 individuals in 59 reference families. Linkage analysis using 28 other markers on human chromosome 1 precisely locates the antiporter gene (locus APNH) on the genetic map of 1 p. The antiporter gene is closely flanked by two highly informative loci, lying 3 cM proximal to the rhesus blood group locus (Rh) and 4 cM distal to the anonymous DNA marker CMM8 (locus D1S79). These antiporter polymorphisms and informative flanking markers will prove useful in genetic linkage studies employing the antiporter gene.

Amiloride↗

A new locus for autosomal dominant "pure" hereditary spastic paraplegia mapping to chromosome 12q13, and evidence for further genetic heterogeneity.

Autosomal dominant pure hereditary spastic paraplegia (ADPHSP) is clinically characterized by slowly progressive lower-limb spasticity. The condition is genetically heterogeneous, and loci have been mapped at chromosomes 2p, 8q, 14q, and 15q. We have performed a genomewide linkage screen on a large family with ADPHSP, in which linkage to all four previously known loci was excluded. Analysis of markers on chromosome 12q gave a peak pairwise LOD score of 3.61 at D12S1691, allowing us to assign a new locus for ADPHSP (a locus that we have designated "SPG10") to this region. Haplotype construction and analysis of recombination events narrowed the SPG10 locus to a 9.2-cM region between markers D12S368 and D12S83. In addition, our data strongly suggest that there are at least six ADPHSP loci, since we describe a further family in which linkage to all five known ADPHSP loci has been excluded.

Adolescent↗

Novel locus for autosomal dominant pure hereditary spastic paraplegia (SPG19) maps to chromosome 9q33-q34.

Hereditary spastic paraplegia is a clinically and genetically heterogeneous disorder characterized by progressive spasticity of the lower limbs. Seven loci for autosomal dominant pure hereditary spastic paraplegia (ADPHSP) have already been mapped on chromosomes 14q, 2p, 15q, 8p, 12q, 19q, and 2q. We report on an Italian family affected by ADPHSP for which we excluded linkage with the known loci and performed a genome-wide search. Linkage analysis and haplotype construction permitted the identification of a novel ADPHSP locus on the long arm of chromosome 9, designated SPG19. The phenotype was characterized by late onset (range, 36-55 years) and mild disability, with only 1 patient bound to a wheelchair after 31 years of disease. Urinary disturbances (urgency and/or incontinence) were always present, even in young patients with a short disease history.

Adolescent↗

hKCNN3 which maps to chromosome 1q21 is not the causative gene in periodic catatonia, a familial subtype of schizophrenia.

The human calcium-activated potassium channel gene (hKCNN3, hSKCa3) contains two tandemly arranged, multiallelic CAG repeats located in exon 1 which result in short to moderate polyglutamine stretches of unknown functional significance. Case-control and family-based association studies suggested an association of hKCNN3 repeats with susceptibility for schizophrenia. Twelve multiplex pedigrees with periodic catatonia, a schizophrenia subtype with major gene effect and patterns of anticipation, were genotyped using the multiallelic hKCNN3 repeat polymorphism. Using a dominant model of inheritance with sex- and age-dependent penetrance classes, cumulative results showed exclusion of linkage of hKCNN3 to periodic catatonia under the assumption of genetic homogeneity with lod score of -48.01 at zero recombination fraction. Our results provide evidence that hKCNN3 is not the causative gene in the familial schizophrenia subtype of periodic catatonia. By fluorescent in situ hybridization we confirmed the assignment of hKCNN3 to chromosome 1q21 near the heterochromatin region. Linkage mapping showed segregation with marker D1S498 (theta = 0.05) and placed hKCNN3 in the genetic linkage map in a cluster of genes near the centromeric region of chromosome 1.

Adult↗

A novel autosomal dominant restless legs syndrome locus maps to chromosome 20p13.

The authors investigated genetic factors contributing to restless legs syndrome (RLS) by performing a 10-cM genome-wide scan in a large French-Canadian pedigree. They detected an autosomal-dominant locus mapping to chromosome 20p13, with a maximum multipoint lod score of 3.86 at marker D20S849. This is the third reported autosomal-dominant locus for RLS and the first autosomal-dominant RLS locus in the French-Canadian population.

Chromosome Mapping↗

Physical mapping of chromosome 21.

Chromosome 21, the smallest human chromosome, has been the subject of intense study because it is the chromosome which, when present in an extra copy, leads to Down Syndrome. Moreover, there are genes important for several human genetic disorders on this chromosome, and a significant number of individuals with aneuploidies of regions of the chromosome have been identified. A high fidelity, high resolution physical map of chromosome 21 will be of immense value in generating an accurate genotype/phenotype map of the chromosome and in identifying and isolating genes on the chromosome which may be responsible for various human genetic disorders. Here we describe the current status of our attempts to create such a map. This includes attempts to integrate various physical mapping approaches. Progress towards construction of a minimal set of yeast artificial chromosomes (YACs) spanning the chromosome is described.

Chromosome Mapping↗