Rapid Mapping of Genomic P1 Clones: The Mousel-Isoaspartyl/d-Aspartyl Methyltransferase Gene

MacLaren, Duncan C.; Clarke, Steven

doi:10.1006/geno.1996.0360

Cited by 5 publications

(3 citation statements)

References 6 publications

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“…of the P1 clone was estimated by restriction digestion of the plasmid DNA with several endonucleases, following the methods of MacLaren & Clarke (1996). The DNA fragments were analyzed using a Field Inversion Gel Electrophoresis (FIGE) Mapper system (BioRad, Hercules, CA, USA), blotted onto nylon membranes (MSI, Westborough, MA, USA), then hybridized with 32 P-labeled probes specific to either side of the insert cloning site of the vector (MacLaren & Clarke 1996).…”

Section: Isolation Of a P1 Clonementioning

confidence: 99%

“…The DNA fragments were analyzed using a Field Inversion Gel Electrophoresis (FIGE) Mapper system (BioRad, Hercules, CA, USA), blotted onto nylon membranes (MSI, Westborough, MA, USA), then hybridized with 32 P-labeled probes specific to either side of the insert cloning site of the vector (MacLaren & Clarke 1996). To verify that both genes were cloned into the P1 plasmid the blots were deprobed then reprobed with 32 P-labeled fulllength (558 bp) relaxin H2 cDNA which recognizes both relaxin genes.…”

Section: Isolation Of a P1 Clonementioning

confidence: 99%

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Analysis of the 5'-upstream regions of the human relaxin H1 and H2 genes and their chromosomal localization on chromosome 9p24.1 by radiation hybrid and breakpoint mapping

Garibay-Tupas¹,

Csiszár²,

Fox³

et al. 1999

Journal of Molecular Endocrinology

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Relaxins are known endocrine and autocrine/ paracrine hormones that play a major role in reproduction. In the human there are two relaxin genes, H1 and H2 which share 90% sequence homology within their coding region. The biological and evolutionary significance of two highly homologous and biologically active human relaxins is unknown. In order to achieve a better understanding of the regulatory mechanisms involved in the differential expression of these two genes and to gain insight into their role(s) in the preterm premature rupture of the membranes, we have investigated the properties of their 5 -upstream regions and mapped them both by radiation hybrid and breakpoint mapping into the same chromosome 9p24·1 locus. The 5 ends of these relaxin genes could be divided into a proximal highly homologous segment and a distal non-homologous region. Within the proximal region are contained several putative regulatory elements common to both genes, suggesting a similar regulatory mechanism. The clustering of the relaxin genes within the same chromosomal locus suggests that these genes may be under a common regulation. On the other hand, a distinct gene-specific regulation may also exist for the individual relaxin genes since cis elements specific to each gene were identified at their 5 ends. Moreover, the observed divergence at the distal region of their 5 -upstream sequences may provide the structural features that act as gene-specific transcription regulators. Since the two genes are highly homologous in both their coding and flanking regions, the divergence at the distal region of their 5 ends may be important in the regulation of these genes and in their involvement in the pathology of preterm birth.

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Section: Isolation Of a P1 Clonementioning

confidence: 99%

Section: Isolation Of a P1 Clonementioning

confidence: 99%

Analysis of the 5'-upstream regions of the human relaxin H1 and H2 genes and their chromosomal localization on chromosome 9p24.1 by radiation hybrid and breakpoint mapping

Garibay-Tupas¹,

Csiszár²,

Fox³

et al. 1999

Journal of Molecular Endocrinology

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“…We constructed a physical map of the P1–106 clone by partial digestion of DNA with Eco RI (MacLaren et al, 1996) (Fig. 1C) and isolated the four genomic DNA probes, PU, A1, P3, and PL (Fig.…”

Section: Resultsmentioning

confidence: 99%

Identification of breakpoint cluster regions at 1p36.3 and 3q21 in hematologic malignancies with t(1;3)(p36;q21)

Shimizu

Suzukawa

Kodera³

et al. 2000

Genes Chromosomes Cancer

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The reciprocal translocation t(1;3)(p36;q21) is associated with myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML) characterized by trilineage dysplasia, in particular dysmegakaryocytopoiesis, and a poor prognosis. As yet no molecular genetic analyses of the t(1;3) have been reported. In four patients with t(1;3), all of whom had AML‐M4, which evolved from MDS, the breakpoints at 3q21 clustered within a 60‐kb region centromeric to the breakpoint of the inv(3)(q21q26), whereas the breakpoints at 1p36 clustered within a 90‐kb region at 1p36.3. The presence of novel clusters in both the 3q21 and 1p36 breakpoints (BCRs) suggests a common, underlying molecular mechanism for the development of t(1;3)‐positive MDS/AML. The Ribophorin I (RPN1) gene close to the BCR at 3q21 was highly expressed without gross structural changes, whereas the GR6 gene located within the BCR at 3q21 was not expressed. No other highly expressed genes were isolated in a 150‐kb region at 3q21. Thus, it is likely that a gene at 1p36.3 is activated by the translocation of the 3q21 region or a gene important for transformation lies on 3q21, outside the 150‐kb region. Further characterization of the BCRs at 1p36.3 and 3q21 should provide important insights into the molecular genetic mechanisms involved in the genesis of t(1;3)‐positive MDS/AML. Genes Chromosomes Cancer 27:229–238, 2000. © 2000 Wiley‐Liss, Inc.

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A deletion on Chromosome 4 cosegregates with the whirler deafness mutation: exclusion of Orm1 as a candidate

Paige

Kiernan

Varela

et al. 2000

Incorporating Mouse Genome

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Whirler (wi) mice display profound deafness and a head-tossing and circling phenotype, showing an autosomal recessive mode of inheritance. The wi mutation has been shown to map close to the Orm gene cluster on mouse Chromosome (Chr) 4. We have, therefore, investigated the Orm loci as candidates for the whirler gene. Detailed mapping and analysis of the Orm gene cluster in both normal and whirler mice indicates the presence of a <48-kb deletion in whirler mice that disrupts the Orm1 locus. The Orm1 locus is also deleted in the CE/J mouse strain, and we discuss the candidature of Orm1 for the whirler gene.

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Rapid Mapping of Genomic P1 Clones: The Mousel-Isoaspartyl/d-Aspartyl Methyltransferase Gene

Cited by 5 publications

References 6 publications

Analysis of the 5'-upstream regions of the human relaxin H1 and H2 genes and their chromosomal localization on chromosome 9p24.1 by radiation hybrid and breakpoint mapping

Analysis of the 5'-upstream regions of the human relaxin H1 and H2 genes and their chromosomal localization on chromosome 9p24.1 by radiation hybrid and breakpoint mapping

Identification of breakpoint cluster regions at 1p36.3 and 3q21 in hematologic malignancies with t(1;3)(p36;q21)

A deletion on Chromosome 4 cosegregates with the whirler deafness mutation: exclusion of Orm1 as a candidate

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