A Strategy for Rapid Construction of Genetic and Physical Maps in the Rat.

Kuramoto, Takashi; Mori, Masayuki; Hirayama, Nobuyuki; Saburi, Sakura; Yamada, Junzo; Serikawa, Tadao

doi:10.1267/ahc.26.325

Cited by 13 publications

(3 citation statements)

References 31 publications

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“…Genotyping of polymorphic markers in the backcrosses and F 2 progeny was performed by using simple sequence length polymorphism (SSLP) markers. The SSLP primers used were produced as described in the previous studies (Serikawa et al 1992;Kuramoto et al 1993;Mathern et al 1994) or obtained from Research Genetics, Inc. (Huntsville, AL, USA). In total, 92 polymorphic markers 1-6 at intervals of approximately 20 centiMorgan (cM) on each chromosome were as follows: Chromosome (Chr) 1: D1Mgh2, Klk1,D1Mgh7,Mt1pa,Pbpc2,D1Mgh14;Chr 2: D2Mgh1,Cpb,Fga,D2Ngh12;Chr 3: D3Mit9,D3Mgh17,D3Mit14,Svs2;Chr 4: D4Mit15,D4Mgh6,Eno2;Chr 5: Penk,D5Mgh6,D5Mit11,Cyp4a2,D5Mgh14,D5Kyo1;Chr 6: D6Mit5,D6Rat107,Rnu1b,D6Mgh4,D6Mgh9,Ighe;Chr 7: D7Mgh11,D7Rat76,D7Mgh7,Myc,Bzrp,Prph;Chr 8: D8Rat55,D8Rat68,Thy1,Apoc3,D8Rat80,D8Rat43,D8Mit2,Cyp1a1,D8N136,D8Mit1,Acaa; Chr 16: D16Mit2,D16Mit3;Chr 17: Chrm3,Hh1tts;…”

Section: Methodsmentioning

confidence: 99%

Genetic analysis of cataract in Ihara epileptic rat

Yokoyama¹,

Amano

Tsuji³

et al. 2001

Mammalian Genome

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We analyzed the mode of inheritance of cataract in the Ihara epileptic rat (IER) by crossing experiments, and mapped cataract-related genes by linkage analysis. Cataract did not develop in the F1 animals, but it developed in both male and female animals of backcross and F2. The occurrence rate of cataract was 48.5% in the backcross progeny and 19.4% in the F2 progeny. Thus, the character was considered to be inherited by the autosomal recessive mode. We found two groups that differed according to the time of onset among the backcross and F2 progeny: an early-onset group (EOG), in which cataracts developed by about 4 months after birth, and a late-onset group (LOG), in which cataracts developed 8 months or more after birth. Linkage analysis indicated the presence of one cataract gene each on Chromosome (Chr) 8 and Chr 15, and the cataract was demonstrated to be governed by more than one gene. The gene on Chr 8 was named Catil, and that on Chr 15. Cati2. Catil was involved in the occurrence of cataract, and the conditions required for cataract to develop were Cati1i/Cati1i or Cati1i/Cati1w. However, in the cataract rats with Cati1i/ Cati1w, the allele of Cati2 was always Cati2i/Cati2i. Cati2 was involved in the timing of onset of the cataract, and the precondition for early onset was Cati2i/Cati2i.

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Section: Methodsmentioning

confidence: 99%

Genetic analysis of cataract in Ihara epileptic rat

Yokoyama¹,

Amano

Tsuji³

et al. 2001

Mammalian Genome

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“…. (1989b, 1990);Serikawa et al (1992b);Kunieda et al (1992a);Kuramoto et al (1993b) Yasne et al (I99t)Falquerho et aL (1991Falquerho et aL ( ) 8erikawa et al (1992b;Remmers et al (1992);Cash et al (1993);Kuramoto et al (1993a);Kondo et aL (1993) Cooke et al (1986;Hilbert et ah (1991); Serikawa et aI. (1992b) Serikawa et al (1992b) Adham et al (1991) Serikawa eta/.…”

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confidence: 99%

A rat genetic linkage map and comparative maps for mouse or human homologous rat genes

1994

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“…Simple sequence length polymorphisms (SSLPs) at Il1b and Prnp were genotyped as described (3,7). Three gene-specific SSLP markers, D3Kur2͞Ptpns1, D3Kur7͞Ptpra, and D3Kur55͞Sn, were developed from the published sequences (GenBank accession numbers D85183, Z36293, and L01702), and two SSLP markers, D3Kur1͞Pdyn and D3Kur9͞Oxt, were developed from the cosmid clones as described (10). While the physical map was assembled (see below), seven anonymous SSLP markers, D3Kur4, D3Kur20, D3Kur24, D3Kur30, D3Kur34, D3Kur37, and D3Kur40, were developed from rat cosmid and P1 clones.…”

Section: Methodsmentioning

confidence: 99%

Attractin/Mahogany/Zitter plays a critical role in myelination of the central nervous system

Kuramoto

Kitada

Inui

et al. 2001

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

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The rat zitter (zi) mutation induces hypomyelination and vacuolation in the central nervous system (CNS), which result in early-onset tremor and progressive flaccid paresis. By positional cloning, we found a marked decrease in Attractin (Atrn) mRNA in the brain of the zi͞zi rat and identified zi as an 8-bp deletion at a splice donor site of Atrn. Atrn has been known to play multiple roles in regulating physiological processes that are involved in monocyte-T cell interaction, agouti-related hair pigmentation, and control of energy homeostasis. Rat Atrn gene encoded two isoforms, a secreted and a membrane form, as a result of alternative splicing. The zi mutation at the Atrn locus darkened coat color when introduced into agouti rats, as also described in mahogany (mg) mice, carrying the homozygous mutation at the Atrn locus. Transgenic rescue experiments showed that the membrane-type Atrn complemented both neurological alteration and abnormal pigmentation in zi͞zi rats, but that the secreted-type Atrn complemented neither mutant phenotype. Furthermore, we discovered that mg mice exhibited hypomyelination and vacuolation in the CNS associated with body tremor. We conclude from these results that the membrane Atrn has a critical role in normal myelination in the CNS and would provide insights into the physiology of myelination as well as the etiology of myelin diseases. T he zitter rat was found in a colony of Sprague-Dawley rats as a tremorous mutant, and subsequent genetic analysis showed that the abnormality was caused by an autosomal recessive gene, zitter (zi) (1, 2). The tremor develops spontaneously at 3 weeks of age, and flaccid paresis of the hind limb is observed at around 6 months of age (3). The main pathological findings are progressive hypomyelination and vacuolation in the central nervous system (CNS) (4). Hypomyelination is characterized by a significant decrease in the density of myelinated fibers and the number of myelin lamellae and is accompanied by aberrant or elongated myelin sheath formation (4). Vacuoles consist mainly of swollen astrocytic processes and enlargement of extracellular space as well as periaxonal spaces. The vacuoles are first detected in the pons and the outer thalamus at 3 weeks of age. With increasing age, vacuoles extend into the deep cortex, hippocampus, cervical spinal gray matter, and the granular layer and white matter of the cerebellum (5). However, the initiation of myelination and the fundamental structures of myelin sheaths are normal in the zitter rat. The biochemical components of myelin, such as myelin basic protein, proteolipid protein, and myelin-associated glycoprotein, are also normally expressed (5, 6). Therefore, the zitter rat is expected to provide useful tools for the study of axon-glia interaction and the assembly of myelin sheaths in the complex process of CNS myelination.The zi gene has been mapped to a genomic region between IL-1␤ (Il1b) and prion protein (Prnp) on rat chromosome (Chr) 3q35 (3, 7). Prnp is known as a causative gene for spongiform ence...

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A Strategy for Rapid Construction of Genetic and Physical Maps in the Rat.

Cited by 13 publications

References 31 publications

Genetic analysis of cataract in Ihara epileptic rat

Genetic analysis of cataract in Ihara epileptic rat

A rat genetic linkage map and comparative maps for mouse or human homologous rat genes

Attractin/Mahogany/Zitter plays a critical role in myelination of the central nervous system

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