Biomedical subjects

Akihiro Kato

Publications and source records attributed to Akihiro Kato.

6 recordsLinked to original sources

PubMed2006

Identification and comparative analysis of the large subunit mitochondrial ribosomal proteins of Neurospora crassa.

The mitochondrial ribosome (mitoribosome) has highly evolved from its putative prokaryotic ancestor and varies considerably from one organism to another. To gain further insights into its structural and evolutionary characteristics, we have purified and identified individual mitochondrial ribosomal proteins of Neurospora crassa by mass spectrometry and compared them with those of the budding yeast Saccharomyces cerevisiae. Most of the mitochondrial ribosomal proteins of the two fungi are well conserved with each other, although the degree of conservation varies to a large extent. One of the N. crassa mitochondrial ribosomal proteins was found to be homologous to yeast Mhr1p that is involved in homologous DNA recombination and genome maintenance in yeast mitochondria.

Humans↗

PubMed2006

[Matrix stone: a case report].

Here, we report a case of matrix stone in a 32-year-old man with diabetes, gout, and chronic renal failure. The patient complained of pain in the left flank. He had undergone an operation for bilateral vesicoureteral reflex at the age of 17 and matrix stone discharge was repeated. Computed tomography revealed a soft tissue mass in the right hydroureter. Percutaneous ureteral lithotripsy was performed successfully. Analysis of the stone components revealed the stone to be composed entirely of protein. Radiological imaging of matrix stones may be difficult to separate from urothelial cancers.

Adult↗

PubMed2005

Growth defect and mutator phenotypes of RecQ-deficient Neurospora crassa mutants separately result from homologous recombination and nonhomologous end joining during repair of DNA double-strand breaks.

RecQ helicases function in the maintenance of genome stability in many organisms. The filamentous fungus Neurospora crassa has two RecQ homologs, QDE3 and RECQ2. We found that the qde-3 recQ2 double mutant showed a severe growth defect. The growth defect was alleviated by mutation in mei-3, the homolog of yeast RAD51, which is required for homologous recombination (HR), suggesting that HR is responsible for this phenotype. We also found that the qde-3 recQ2 double mutant showed a mutator phenotype, yielding mostly deletions. This phenotype was completely suppressed by mutation of mus-52, a homolog of the human KU80 gene that is required for nonhomologous end joining (NHEJ), but was unaffected by mutation of mei-3. The high spontaneous mutation frequency in the double mutant is thus likely to be due to NHEJ acting on an elevated frequency of double-strand breaks (DSBs) and we therefore suggest that QDE3 and RECQ2 maintain chromosome stability by suppressing the formation of spontaneous DSBs.

Adenosine Triphosphatases↗

PubMed2005

Srs2 and RecQ homologs cooperate in mei-3-mediated homologous recombination repair of Neurospora crassa.

Homologous recombination and post-replication repair facilitate restart of stalled or collapsed replication forks. The SRS2 gene of Saccharomyces cerevisiae encodes a 3'-5' DNA helicase that functions both in homologous recombination repair and in post-replication repair. This study identifies and characterizes the SRS2 homolog in Neurospora crassa, which we call mus-50. A knockout mutant of N.crassa, mus-50, is sensitive to several DNA-damaging agents and genetic analyses indicate that it is epistatic with mei-3 (RAD51 homolog), mus-11 (RAD52 homolog), mus-48 (RAD55 homolog) and mus-49 (RAD57 homolog), suggesting a role for mus-50 in homologous recombination repair. However, epistasis evidence has presented that MUS50 does not participate in post-replication repair in N.crassa. Also, the N.crassa mus-25 (RAD54 homolog) mus-50 double mutant is viable, which is in contrast to the lethal phenotype of the equivalent rad54 srs2 mutant in S.cerevisiae. Tetrad analysis revealed that mus-50 in combination with mutations in two RecQ homologs, qde-3 and recQ2, is lethal, and this lethality is suppressed by mutation in mei-3, mus-11 or mus-25. Evidence is also presented for the two independent pathways for recovery from camptothecin-induced replication fork arrest: one pathway is dependent on QDE3 and MUS50 and the other pathway is dependent on MUS25 and RECQ2.

DNA Helicases↗

PubMed2004

[CT findings of pulmonary hamartoma with special reference to epithelial-lined clefts and connection with pulmonary arteries].

PURPOSE: The purpose of this study was to clarify the characteristic CT findings of pulmonary hamartoma. MATERIALS AND METHODS: The thin-section CT and multiplanar reformation images of 19 pulmonary hamartomas diagnosed by surgical resection were analyzed and correlated with the pathological findings. RESULTS: Most hamartomas presented lobulated nodules apart from pleura. There was no case in which fat density was recognized. Only one case was recognized as having calcification. Air density in the connection of the side or the inside was pointed out in 5 cases (26%). Air density reflected epithelial-lined cleft. The connection with the bronchus was recognized in 4 cases (21%), and the connection with the pulmonary artery branch was recognized in 10 cases (53%). However, the connection of the pulmonary artery and bronchus could not be pathologically confirmed in most cases. The connection with the pulmonary vein was not recognized in any of the cases. CONCLUSION: Air density in the connection of the side or the inside is characteristic of pulmonary hamartoma. Pulmonary artery branches connect beyond half of hamartomas. This finding suggests close relations in the bronchus along the artery. It is important that there is no connection of the pulmonary vein, to differentiate it from lung cancer.

Calcinosis↗

PubMed2003

The Neurospora crassa mus-19 gene is identical to the qde-3 gene, which encodes a RecQ homologue and is involved in recombination repair and postreplication repair.

An allele called mus-19 was identified by screening temperature-sensitive and mutagen-sensitive mutants of Neurospora crassa. The mus-19 gene was genetically mapped to a region near the end of the right arm of linkage group I, where a RecQ homologue called qde-3 had been physically mapped in the Neurospora database. Complementation tests between the mus-19 mutant and the qde-3(RIP) mutant showed that mus-19 and qde-3 were the same gene. The qde-3 genes of both mutants were cloned and sequenced; and the results showed that they have mutation(s) in their qde-3 genes. The original mus-19 and qde-3(RIP) mutants are defective in quelling, as reported for other qde-3 mutants. The mutants show high sensitivity to methyl methanesulfonate, ethyl methanesulfonate, N-methyl- N'-nitro- N-nitrosoguanidine, tert-butyl hydroperoxide, 4-nitroquinoline-1-oxide, hydroxyurea and histidine. Epistasis analysis indicated that the qde-3 gene belongs both to the uvs-6 recombination repair pathway and the uvs-2 postreplication repair pathway. The qde-3 mutation has no effect on the integration of a plasmid carrying the mtr gene by homologous recombination. In homozygous crosses, the qde-3 mutant is defective in ascospore production.

Adenosine Triphosphatases↗