The human mitochondrial ribosomal protein genes: mapping of 54 genes to the chromosomes and implications for human disorders.

Mitochondria possess their own translational machinery, which is composed of components distinct from their cytoplasmic counterparts. To investigate the possible involvement of mitochondrial ribosomal defects in human disease, we mapped nuclear genes that encode mitochondrial ribosomal proteins (MRPs). We generated sequence-tagged sites (STSs) of individual MRP genes that were able to be detected by PCR. They were placed on an STS content map of the human genome by typing of radiation hybrid panels. We located 54 MRP genes on the STS-content map and assigned these genes to cytogenetic bands of the human chromosomes. Although mitochondria are thought to have originated from bacteria, in which the genes encoding ribosomal proteins are clustered into operons, the mapped MRP genes are widely dispersed throughout the genome, suggesting that transfer of each MRP gene to the nuclear genome occurred individually. We compared the assigned positions with candidate regions for mendelian disorders and found certain genes that might be involved in particular diseases. This map provides a basis for studying possible roles of MRP defects in mitochondrial disorders.

A complete map of the human ribosomal protein genes: assignment of 80 genes to the cytogenetic map and implications for human disorders.

Mapping of the human ribosomal protein (RP) genes has been completed, and all 80 different genes were placed on a cytogenetic map of the human genome. Because of the existence of processed pseudogenes, the localization of the RP genes was complicated, and five genes had remained to be mapped. Here we developed a novel strategy to identify sequence-tagged sites (STSs) at introns of the RP genes, and we localized RPL14, RPL22, RPL35, RPL36, and RPL39 within the chromosomes by radiation hybrid mapping. Unlike the case of eubacteria or archaebacteria, human RP genes are widely scattered about the genome. Together with the previous results, both sex chromosomes and 20 autosomes (all but chromosomes 7 and 21) were found to carry one or more RP genes. To explore the possible involvement of RP genes in human disorders, all 80 genes were assigned to cytogenetic bands according to a published cytogenetic BAC-STS map of the human genome. We compared the assigned positions with candidate regions for Mendelian disorders and found certain genes that might be involved in particular human disorders.

Survey of tick infestation and tick-borne ehrlichial infection of dogs in Ishigaki Island, Japan.

Twelve (54.5%) of 22 free-roaming dogs in Ishigaki Island had tick infestation identified as Rhipicephalus sanguineus. There were 121 ticks recovered and consisted of 28 females, 58 males, 22 nymphs and 3 larvae. Infection of dogs possibly with canine ehrlichial pathogens was examined by both indirect immunofluorescence assay and polymerase chain reaction (PCR). Two dogs of the 13 examined were sero-positive for the human granulocytic ehrlichia agent, and one of two dogs was PCR positive for Ehrlichia platys. This dog had platelet numbers slightly lower than normal value, however, no morulae were found within platelet on peripheral blood smear stained with Giemsa.

Larvicidal activity of the symbiotic bacterium Xenorhabdus japonicus from the entomopathogenic nematode Steinernema kushidai against Anomala cuprea (Coleoptera:Scarabaeidae).

The entomopathogenicity of the symbiotic bacterium Xenorhabdus japonicus and the nematode Steinernema kushidai was determined. Phase I and II X. japonicus were cultured on an artificial medium and inoculated into the test insect or established into axenic S. kushidai populations. When 100, 1000, or 10,000 bacterial cells of phase I or II were directly injected into the hemocoels of 3rd instar cupreous chafer, Anomala cuprea, both phases in the late log period killed 100% of the larvae by the 2nd day postinoculation. However, both phases in the stationary period were less pathogenic with cupreous chafer mortality < 20 and 80% at 100 and 1000 bacterial cells/ larva, respectively. In vitro studies showed that axenic S. kushidai provided with phase I or II symbionts grew well and produced equal numbers of progeny on a dog food medium, but nematodes with no symbionts did not grow at all. Pig liver extracts added as a dietary supplement to the dog food medium completely restored growth and progeny production of the nematode with no bacterial cells. Studies were conducted with infective juveniles (IJs) harboring phase I or II or no symbionts that were applied against 3rd instar cupreous chafer larvae in compost or injected directly into their hemocoels. In the compost study, IJs harboring phase I killed 100% within 10 days. IJs with phase II or no symbionts caused low mortality of the cupreous chafer larvae at 10 days (< 20%). In the intrahemocoelic injection study, IJs harboring phase I resulted in 60% larval mortality at five nematodes/larva, and as the number of IJs injected increased, significantly higher larval mortality was obtained.