Mouse Chromosome 8

Ceci, Jeffrey D.; Lusis, Aldons J.

doi:10.1007/bf00648426

Cited by 5 publications

(3 citation statements)

References 98 publications

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“…Human PLCGI and PLCG2 could be assigned to Chrs 20 and 16, as expected from their positions on mouse Chr 2 and Chr 8 respectively (Siracusa and Abbott 1994;Ceci 1994). Although the location of PLCD1 was predicted to be human Chr 8 from its previously described homology to this region of mouse Chr 8 (Ceci 1994), our data place PLCD1 on human Chr 3. Human Chr 8 was excluded, since three hybrids (803, 81 l, and 909) contained Chr 8 but not PLCD1, and two hybrids (423, 1079) contained PLCD1, but not Chr 8.…”

Section: Resultssupporting

confidence: 68%

“…Human PLCD3 and PLCD4 mapped to Chr 17 and 2, which contain regions of conserved synteny with mouse Chr 11 and Chr 2, respectively (Lossie et al 1994;Siracusa and Abbott 1994). Human PLCGI and PLCG2 could be assigned to Chrs 20 and 16, as expected from their positions on mouse Chr 2 and Chr 8 respectively (Siracusa and Abbott 1994;Ceci 1994). Although the location of PLCD1 was predicted to be human Chr 8 from its previously described homology to this region of mouse Chr 8 (Ceci 1994), our data place PLCD1 on human Chr 3.…”

Section: Resultsmentioning

confidence: 89%

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Genetic mapping of the human and mouse phospholipase C genes

et al. 1996

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To determine chromosome positions for 10 mouse phospholipase C (PLC) genes, we typed the progeny of two sets of genetic crosses for inheritance of restriction enzyme polymorphisms of each PLC. Four mouse chromosomes, Chr 1, 11, 12, and 19, contained single PLC genes. Four PLC loci, Plcb1, Plcb2, Plcb4, and Plcg1, mapped to three sites on distal mouse Chr 2. Two PLC genes, Plcd1 and Plcg2, mapped to distinct sites on Chr 8. We mapped the human homologs of eight of these genes to six chromosomes by analysis of human x rodent somatic cell hybrids. The map locations of seven of these genes were consistent with previously defined regions of conserved synteny; Plcd1 defines a new region of homology between human Chr 3 and mouse Chr 8.

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Section: Resultssupporting

confidence: 68%

Section: Resultsmentioning

confidence: 89%

Genetic mapping of the human and mouse phospholipase C genes

et al. 1996

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“…The mouse map location of the pogo locus appears to place it in a region homologous to human 4q31-q31 (Ceci and Mills 1998). One of the candidate genes for the pogo gene is chloride channel 3 (Clcn3) that lies within 1 cM of D8Mit128, according to the consensus map positions (Grewal et al 1997).…”

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confidence: 99%

Mapping of the pogo gene, a new ataxic mutant from Korean wild mice, on central mouse Chromosome 8

et al. 2001

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Three male mice of Korean wild stock, named KJR/MsKist, exhibiting abnormal behavior were discovered in November 1995. They were mated to normal sib females, and brother-sister mating was continued. Affected mice showing ataxia were recovered in the succeeding generations. These were characterized by a wobbly gait and a tendency to fall over, which appeared at about 2 weeks of age and continued throughout life. There was no further progression of the phenotype with age. The mutant strain was named POGO/Kist and maintained at the Korea Research Institute of Bioscience and Biotechnology.Four behavior tests were designed to characterize the abnormalities of the POGO/Kist mice. Results of these behavior tests are summarized in Table 1. The still-rod test was performed to see whether the affected mice had a deficiency in motor coordination. Endurance time for animals standing on a stationary rod (diameter 2.5 cm, length 25 cm) was measured for 2 min, the upper limit. The difference in the endurance times of normal and affected mice was recorded. All of the normal animals stayed on the still-rod for 2 min, whereas affected mice fell from the still-rod within 7 s (Table 1). This result was taken as evidence that mutant mice have motor coordination defects.A glass beaker (diameter 11 cm, height 14.5 cm) was used as a means of observing rearing behavior, as mice tend to rear when restricted. The mean distance between the hind paws was measured to assess any abnormality of the hind limbs, and this was determined to be 25.71 mm in normal mice. Two of the six affected mice could not rear at all, and the corresponding mean distance in the other 4 mice was 53.75 mm (Table 1). Their haunches touched the bottom of the beaker as they reared, even for a short time. This observation demonstrates that the development of motor coordination in the hind limbs is insufficient to maintain a rearing posture, which is surprising in view of the fact that there were no significant differences between the affected and normal mice in either the general activity test or the open field test. The rotor-rod test was not used because affected mice dropped too quickly from the rotor-rod. These behavioral patterns suggest that affected mice may have motor coordination abnormalities.To determine the pathological defects in the affected mice, we examined the brain, spinal cord, and muscles. The spinal cord and muscles of the hind limbs were normal on gross examination. However, abnormalities were observed in the cerebellum by immunohistochemical staining for calbindin-D. Calbindin is a 28-kDa protein that is expressed in the cerebellum exclusively by Purkinje cells (De Camilli et al. 1984;Ozol et al. 1999). Anticalbindin immunocytochemistry showed deposited peroxidase reaction product throughout all Purkinje cells, including the somata, dendrites, dendritic spines, and axons, in both normal wild-type and affected mutant mice. The cross-sectioned Purkinje cell dendrites of affected mice were larger than those of normal mice (Fig. 1).Genetic analyses wer...

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