A radiation hybrid map of the rat genome containing 5,255 markers

Watanabe, Takeshi; Bihoreau, Marie Thérèse; McCarthy, Linda; Kiguwa, Susanna L.; Hishigaki, Haretsugu; Tsuji, Atsushi B.; Browne, Julie; Yamasaki, Yoshio; Mizoguchi-Miyakita, Ayako; Oga, Keiko; Ono, Toshihide; Okuno, Shiro; Kanemoto, Naohide; Takahashi, Ei; Tomita, Kazuhiro; Hayashi, Hiromi; Adachi, Masakazu; Webber, Caleb; Davis, M.; Kiel, Susanne; Knights, Catherine; Smith, A.C.; Critcher, Ricky; Miller, Jonathan; Thangarajah, T.; Day, Philip J.; Hudson, James R.; Irie, Yasuo; Takagi, Toshihisa; Nakamura, Yusuke; Goodfellow, Peter N.; Lathrop, G.M.; Tanigami, Akira; James, M. R.

doi:10.1038/8737

Cited by 218 publications

(214 citation statements)

References 43 publications

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“…Similar clustering of SSR markers was also reported in the tomato (Broun and Tanksley 1996;Areshchenkova and Ganal 1999) and rice linkage maps (McCouch et al 2003). Physical clustering of SSR markers was also reported in the rat radiation hybrid map (Watanabe et al 1999) and in barley . Morgante et al (2002) and Cardle et al (2000) indicated that microsatellites are significantly associated with the low-copy fraction of plant genomes based on the estimation of microsatellite density in Arabidopsis thaliana, rice, soybean, maize, and wheat.…”

Section: Discussionmentioning

confidence: 67%

A new integrated genetic linkage map of the soybean

Song¹,

et al. 2004

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Section: Discussionmentioning

confidence: 67%

A new integrated genetic linkage map of the soybean

Song¹,

et al. 2004

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“…Statistical analyses show significant differences in astrogliosis and myelination defects between the 2 species ( * , P Ͻ 0.05 and *** , P Ͻ 0.001). mouse, and human genomes encode similar numbers of genes (19)(20)(21)(22)(23). Therefore, we suggest that differences in genetic background between mice and rats may be one possible explanation for the neuroprotective effect of hypoxia in mice but not in rats.…”

Section: Discussionmentioning

confidence: 99%

Vulnerability of white matter towards antenatal hypoxia is linked to a species-dependent regulation of glutamate receptor subunits

Fontaine

Olivier

Massonneau

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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White-matter damage is a leading cause of neurological handicap. Although hypoxia-ischemia and excitotoxicity are major pathogenic factors, a role for genetic influences was suggested recently. Thus, protracted gestational hypoxia was associated with whitematter damage (WMD) in rat pups but not in mouse pups. Indeed, microglial activation and vessel-wall density on postnatal days (P)1 and P10 were found increased in both mouse and rat pups, but cell death, astrogliosis, and myelination were only significantly altered in hypoxic rat pups. We investigated whether this species-related difference was ascribable to effects of antenatal hypoxia on the expression of glutamate receptor subunits by using immunocytochemistry, PCR, and excitotoxic double hit insult. Quantitative PCR in hypoxic mouse pups on P1 showed 2-to 4-fold down-regulation of the AMPA-receptor subunits -1, 2, and -4; of the kainate-receptor subunit GluR7; and of the metabotropic receptor subunits mGluR1, -2, -3, -5, and -7. None of the glutamate-receptor subunits was down-regulated in the hypoxic rat pups. NR2B was the only NMDA-receptor subunit that was down-regulated in hypoxic mice but not in hypoxic rat on P1. Ifenprodil administration to induce functional inhibition of NMDA containing NR2B-subunit receptors prevented hypoxia-induced myelination delay in rat pups. Intracerebral injection of a glutamate agonist produced a larger decrease in ibotenate-induced excitotoxic lesions in hypoxic mouse pups than in normoxic mouse pups. Gestational hypoxia may regulate the expression of specific glutamate-receptor subunits in fetal mice but not in fetal rats. Therefore, genetic factors may influence the susceptibility of rodents to WMD. brain damage ͉ NMDA receptors ͉ genetic factors ͉ development ͉ prematurity P eriventricular (P) WMD and subsequent cortical damage are the leading causes of cerebral palsy (CP) limited to preterm birth (1, 2). Animal models have been developed to unravel the mechanisms underlying these brain lesions. Factors that seem involved in the pathophysiology of CP in these models include hypoxia and ischemia, infection and inflammation, excitotoxicity, accumulation of reactive oxygen species, and deficiencies in growth factors (3, 4). These factors seem to act in combination to cause damage to the developing white matter.Glutamate accumulation may be a mechanism common to many risk factors for CP. Glutamate, the major excitatory neurotransmitter, acts by means of several groups of receptors, namely, NMDA, AMPA, kainate, and metabotropic receptors (mGluRs). Excessive activation of glutamate receptors may cause cell vulnerability, in part as a result of intracellular calcium influx (5, 6). Intracerebral injection of glutamate agonists into the neocortex and white matter of newborn rodents produces histological lesions that mimic the brain damage observed in preterm neonates (7-10).Several studies suggest that genetic factors may influence the susceptibility of very preterm infants to PWMD. The occurrence of CP may depend, at least in ...

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“…Interestingly, the polymorphic nature of Ncl Z1 has been previously used in genetic mapping, and it is known as marker D9Arb5 on rat chromosome 9 (29). Many of the polymorphic dinucleotide repeats used in genetic mapping consist of alternating purine͞pyrimidine repeats and thus have the potential to form Z-DNA.…”

Section: Discussionmentioning

confidence: 99%

A polymorphic dinucleotide repeat in the rat nucleolin gene forms Z-DNA and inhibits promoter activity

Rothenburg

Koch-Nolte

Rich

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

131

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Many sequences in eukaryotic genomes have the potential to adopt a left-handed Z-DNA conformation. We used a previously described assay based on the binding of a mAb to Z-DNA to inquire whether Z-DNA is formed in the rat nucleolin (Ncl) gene in metabolically active, permeabilized nuclei. Using real-time PCR to measure Z-DNA formation, the potential Z-DNA sequence element Z1 [(CA) 10(CG)8] in the promoter region was found to be enriched 571-to 4,040-fold in different cell lines, whereas Z2 [AC(GC) 5CCGT(CG)2] in the first intron was enriched 12-to 34-fold. Ncl promoter activity was 1.5-to 16-fold stronger than that of the simian virus 40 promoter and enhancer. This activity was further increased 36 -54% when Z1 was deleted. The inhibitory effect of Z1 on Ncl promoter activity was independent of location and orientation. The Ncl Z1 element is identical to the genetic marker D9Arb5. Five allelic variants of Z1 were identified by sequence analysis of genomic DNA from various rats. The two most common alleles differed significantly (up to 27%) in their capacity to inhibit Ncl promoter activity. This finding suggests that differences in Z-DNA formation by polymorphic dinucleotide repeats may be one of the factors contributing to genetic variation.gene regulation ͉ polymorphism ͉ microsatellites ͉ left-handed DNA D inucleotide repeats are found throughout the genome of eukaryotes. (CA͞TG) n is the most abundant one in mammals, found on average every 20-30 kb (1). These microsatellites often are polymorphic and have been used extensively in genetic mapping and the identification of susceptibility loci in genetic diseases (2). Evidence is accumulating that such elements also can be of functional importance. Dinucleotide repeats have the potential to form alternative DNA structures such as Z-DNA, H-DNA, and cruciform DNA (3, 4). One of the bestcharacterized alternative DNA conformations is left-handed Z-DNA, which can be adopted by stretches of alternating purine-pyrimidine nucleotides.Z-DNA formation of many sequences can be induced in vitro (5). (CG) n repeats have the highest potential to form Z-DNA, followed by (CA͞TG) n and (TA) n (5). Sequences containing alternating purine-pyrimidine nucleotides have been shown to modulate promoter activity. They may either enhance (6, 7) or repress (8) promoter activity. Because of the polymorphic nature of dinucleotide repeats, it seems possible that Z-DNA-forming sequences may provide a source of genetic variation if they occur in regions that are important for the regulation of gene activity.An assay based on the preparation of metabolically active nuclei, introduced by Jackson and Cook (9), has been developed to investigate whether specific potential Z-DNA-forming sequences actually adopt this conformation in actively transcribing eukaryotic genes (10). These nuclei maintain transcription and show a DNA replication rate of 85%, compared with untreated cells (11). The permeable nuclei are incubated with a biotinylated mAb specific for Z-DNA. A 10-ns laser pulse at 266 nm is use...

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A radiation hybrid map of the rat genome containing 5,255 markers

Cited by 218 publications

References 43 publications

A new integrated genetic linkage map of the soybean

A new integrated genetic linkage map of the soybean

Vulnerability of white matter towards antenatal hypoxia is linked to a species-dependent regulation of glutamate receptor subunits

A polymorphic dinucleotide repeat in the rat nucleolin gene forms Z-DNA and inhibits promoter activity

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