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T Toda

Publications and source records attributed to T Toda.

At least 109 records · Page 6Linked to original sources
PubMed1999

A simple hydroponic culture method for the development of a highly viable root system in Arabidopsis thaliana.

In the studies of nutritional absorption and metal toxicity in the root, it is important to grow plants without technical damage. We established a simple hydroponic culture system for Arabidopsis thaliana to obtain a healthy plant having a well-developed root system with many lateral roots. The phytotoxic effects of Cr, Cu, and Al ions were examined by FDA-PI staining using this culture system. The pattern of root inhibition varied with the ion, suggesting the usefulness of this culture system.

Aluminum↗
PubMed1999

Apolipoprotein A-I of hyperlipidemia atherosclerosis prone (LAP) quail: cDNA sequence and tissue expression.

Apolipoprotein A-I (apo A-I) has an important role in the transport of cholesterol. This study describes the complete nucleotide and deduced amino acid sequence for apo A-I of LAP quail. A full length apo A-I cDNA clone for hyperlipidemia atherosclerosis prone (LAP) quail was isolated from a lambda gt10 liver cDNA library. The DNA sequence of LAP apo A-I cDNA was similar to that of normal Japanese quail. The deduced amino acid sequence of LAP apo A-I was hence identical to that of normal Japanese quail. LAP apo A-I mRNA is about 1.4 kilobases in length and expressed in a variety of tissues including small intestine, liver, lung, breast muscle, testis, and heart. Although the tissue distribution of apo A-I was similar between strains, LAP quail expressed more apo A-I mRNA than normal Japanese quail in all tissues examined. This tendency was pronounced with the small intestine. Although the concentration of serum apo A-I did not correlate with the tissue expression of mRNA, the observation may suggest that the increased apo A-I expression in LAP strain had some relevance to the susceptibility of this strain to the experimental atherosclerosis.

Amino Acid Sequence↗
PubMed1999

Sarcoidosis with membranous nephropathy and granulomatous interstitial nephritis.

A 49-year-old woman, who had been diagnosed as sarcoidosis based on bilateral hilar lymphadenopathy and lung biopsy, presented increased serum creatinine and calcium concentrations. Renal biopsy showed the presence of interstitial nephritis with non-caseating epithelioid granuloma and focal membranous transformation. Therapy with prednisolone was effective in normalizing serum creatinine, serum calcium, serum angiotensin converting enzyme, and urine beta2 microglobulin, but these abnormalities reappeared after rapid withdrawal of prednisolone. This is a rare case of sarcoidosis manifested by both membranous nephropathy and granulomatous interstitial nephritis, and indicates the necessity of long-term treatment of corticosteroid.

Female↗
PubMed1999

[Genetic alterations in human malignant tumor].

To clarify the genetic background of cancer patients, microsatellite instability (MSI) and mutations of transforming growth factor-beta type II receptor (RII), p53 and k-ras gene were investigated. MSI were detected in 33.3% of esophageal, 15.8% of gastric, 21.4% of colorectal, 4.5% of bile duct, 0% of gallbladder, 13.3% of pancreatic, 11.6% of breast and 10.5% of thyroid cancers. Mutations of RII gene were detected in only 2 of 9 MSI-positive colorectal cancers. k-ras gene mutations were investigated in colorectal, bile duct, gallbladder, breast and thyroid cancer and were detected in 11.9%, 36.4%, 64.3%, 0%, 0% of each. p53 gene mutations were investigated in colorectal and breast cancer and were detected in 9.5% and 9.3%, respectively. In addition, 4 colorectal cancer cases exhibited more than two kinds of genetic alteration, while breast cancer cases showed only single kind. From these findings, it is suggested that 1) the incidence of each genetic alteration differed among the cancers investigated and organ specificity may exist; 2) the genetic alterations investigated here contributed to a minor part of cancer development, which requires the identification of more unknown genes related to carcinogenesis; 3) to clarify the molecular mechanism of cancer development, the genetic alterations including genomic instability and mutations of several kinds of genes related to cancer development in each case should also be determined along with their genetic molecular profile.

Genes, p53↗
PubMed1999

Novel (CA)n marker DXYS241 on the nonrecombinant part of the human Y chromosome.

The origin of modern humans can be traced by comparing polymorphic sites in either mitochondria or genomic sequences between humans and other primates. The human Y chromosome has both a non-recombining region and X-Y homologous pseudo-autosomal regions. In the nonrecombining region events during evolution can be directly detected. At least a part of homology between Xq21 and Yp11 is a result of rather recent translocations from the X chromosome to the Y chromosome. DNA markers residing in the nonrecombining region of the human Y chromosome are potentially useful in tracing male-specific gene flow in human evolution. However, the number of available markers in the region is limited. Here, we report a novel X-Y homologous (CA)n repeat locus in the nonrecombining region of the Y chromosome. This marker, DXYS241, has several interesting features. Y- and X-chromosome alleles are distinguishable because the Y-chromosome alleles are shorter than the X-chromosome alleles most of the time. We developed 2 primer sets for specific examination of Y- and X-chromosome alleles. The marker should be useful in establishing relationships between populations based on patrilineal gene flow. Sequences homologous to DXYS241 are also found on the X chromosome of primates. Four events during primate evolution that led to the modern human Y chromosome were identified.

Alleles↗
PubMed1999

[A patient of Walker-Warburg syndrome with a haplotype different from that in Fukuyama-type congenital muscular dystrophy].

A 3-month-old female baby was diagnosed as having Walker-Warburg syndrome (WWS), based on the following clinical findings: type II lissencephaly associated with marked ventricular dilatation, cerebellar malformation, retinal malformation, elevated serum creatine kinase level and abnormal muscle CT findings. She was a product of parents with consanguineous marriage. She presented with severe hypotonia and profound psychomotor retardation since birth. She developed infantile spasms at 8 months of age, and vitamin B6 was very effective. A genetic analysis revealed the absence of the founder haplotype commonly seen in Fukuyama-type congenital muscular dystrophy (FCMD), suggesting that the WWS gene is not always identical to the FCMD gene. When she was examined at the age of 4 years, she had no apparent further psychomotor development. Her clinical symptoms were more severe than those of the typical FCMD.

Abnormalities, Multiple↗
PubMed1998

Age dependent decline in the 3'-->5' exonuclease activity involved in proofreading during DNA synthesis.

A 3'-->5' exonuclease found in rat liver excises mispaired nucleotides at the 3'-hydroxyl end of primer chains such as poly dA-d(T9-C). Consequently, the priming activity of the chain from which the mispaired base was cut is greatly increased during DNA synthesis. These results suggest that the 3'-->5' exonuclease acts as a proofreading enzyme during DNA synthesis. The activity of this 3'-->5' exonuclease in the liver of 24-month-old rats is approximately 30% lower than the activity found in 4-month-old rats. Furthermore, non-complementary nucleotide incorporations by DNA polymerases from aged rats are observed during DNA synthesis on poly dA-dT10. The number of misincorporations decreases in the presence of the 3'-->5' exonuclease, but not all errors are prevented even when DNA polymerase and 3'-->5' exonuclease are added at an activity ratio similar to that found in vivo. The data suggest that declines in both the fidelity of DNA polymerase and the 3'-->5' exonuclease activity related to proofreading during the aging process lead to a higher frequency of base misincorporations during DNA replication.

Aging↗
PubMed1998

Apc10 and Ste9/Srw1, two regulators of the APC-cyclosome, as well as the CDK inhibitor Rum1 are required for G1 cell-cycle arrest in fission yeast.

Many eukaryotic cells arrest the cell cycle at G1 phase upon nutrient deprivation. In fission yeast, during nitrogen starvation, cells divide twice and arrest at G1. We have isolated a novel type of sterile mutant, which undergoes one additional S phase upon starvation and, as a result, arrests at G2. Three loci (apc10, ste9/srw1 and rum1) were identified. The apc10 mutants, previously unidentified, show, in addition to sterility, temperature-sensitive growth with defects in chromosome segregation. apc10(+) is essential for viability, encodes a conserved protein (a homologue of budding yeast Apc10/Doc1) and is required for ubiquitination and degradation of mitotic B-type cyclins. Apc10 does not co-sediment with the 20S APC-cyclosome, a ubiquitin ligase for B-type cyclins, and in the apc10 mutant the 20S complex is intact, suggesting that it is a novel regulator for this complex. A subpopulation of Apc10 does co-immunoprecipitate with the anaphase-promoting complex (APC). A second gene, ste9(+)/srw1(+), encodes a member of the fizzy-related family, also regulators of the APC. Finally, Rum1 is a cyclin-dependent kinase (CDK) inhibitor which exists only in G1. The results suggest that dual downregulation of CDK, one via the APC and the other via the CDK inhibitor, is a universal mechanism that is used to arrest cell cycle progression at G1.

Amino Acid Sequence↗
PubMed1998

Crystallographic characterization of Pap1-DNA complex.

Pap1 is a fission yeast transcription factor that activates genes related with resistance against staurosporine, a potent inhibitor of protein kinase C, and has been shown to be involved in cell growth, cell cycle, carcinogenesis and differentiation. Pap1 has the bZIP DNA-binding domain but binds to non-consensus DNA sequences for the bZIP motif. Highly ordered crystals of the DNA-binding domain complexed with a DNA fragment that has an ATF/CREB-like non-consensus sequence have been obtained. The crystals grew by the vapor-diffusion technique with polyethylene glycol 6000 and belong to space group R3 with a = b = 240.78, c = 43.85 A. A 2.0 A resolution data set was collected with a cryo-crystallographic technique.

Basic-Leucine Zipper Transcription Factors↗
PubMed1998

An ancient retrotransposal insertion causes Fukuyama-type congenital muscular dystrophy.

Fukuyama-type congenital muscular dystrophy (FCMD), one of the most common autosomal recessive disorders in Japan (incidence is 0.7-1.2 per 10,000 births), is characterized by congenital muscular dystrophy associated with brain malformation (micropolygria) due to a defect in the migration of neurons. We previously mapped the FCMD gene to a region of less than 100 kilobases which included the marker locus D9S2107 on chromosome 9q31. We have also described a haplotype that is shared by more than 80% of FCMD chromosomes, indicating that most chromosomes bearing the FCMD mutation could be derived from a single ancestor. Here we report that there is a retrotransposal insertion of tandemly repeated sequences within this candidate-gene interval in all FCMD chromosomes carrying the founder haplotype (87%). The inserted sequence is about 3 kilobases long and is located in the 3' untranslated region of a gene encoding a new 461-amino-acid protein. This gene is expressed in various tissues in normal individuals, but not in FCMD patients who carry the insertion. Two independent point mutations confirm that mutation of this gene is responsible for FCMD. The predicted protein, which we term fukutin, contains an amino-terminal signal sequence, which together with results from transfection experiments suggests that fukutin is a secreted protein. To our knowledge, FCMD is the first human disease to be caused by an ancient retrotransposal integration.

Amino Acid Sequence↗
PubMed1998

Prenatal diagnosis of Fukuyama type congenital muscular dystrophy in eight Japanese families by haplotype analysis using new markers closest to the gene.

We conducted prenatal diagnosis by haplotype analysis, using newly developed microsatellite markers, in eight Fukuyama type congenital muscular dystrophy (FCMD) families. In addition to six new families, two previously reported families were reexamined by haplotype analysis including detection of an ancestral founder haplotype (138-183-301) for 3 microsatellite markers closest to the FCMD gene, designated D9S2105-D9S2107-D9S172, the distances of which from the FCMD gene are presumed to be approximately 140, approximately 20, and approximately 280 kb, respectively. Five fetuses from five families were diagnosed as nonaffected, and were subsequently confirmed to be healthy. Three fetuses of the other three families were diagnosed as having a high probability of being affected by FCMD. In the prenatal diagnosis conducted for these eight families, the ancestral founder allele was observed in 13 of 16 (81%) FCMD-bearing chromosomes. Detection of the ancestral haplotype facilitated achieving accurate prenatal diagnosis of FCMD. The brains of all three fetuses prenatally diagnosed as FCMD-affected showed the initial stage of cortical dysplasia, strong evidence of FCMD.

Brain↗
PubMed1998

Regulation of the fission yeast transcription factor Pap1 by oxidative stress: requirement for the nuclear export factor Crm1 (Exportin) and the stress-activated MAP kinase Sty1/Spc1.

The fission yeast Sty1 stress-activated MAP kinase is crucial for the cellular response to a variety of stress conditions. Accordingly, sty1- cells are defective in their response to nutrient limitation, lose viability in stationary phase, and are hypersensitive to osmotic stress, oxidative stress, and UV treatment. Some of these phenotypes are caused by Sty1-dependent regulation of the Atf1 transcription factor, which controls both meiosis-specific and osmotic stress-responsive genes. However, in this report we demonstrate that the cellular response to oxidative stress and to treatment with a variety of cytotoxic agents is the result of Sty1 regulation of the Pap1 transcription factor, a bZip protein with structural and DNA binding similarities to the mammalian c-Jun protein. We show that both Sty1 and Pap1 are required for the expression of a number of genes involved in the oxidative stress response and for the expression of two genes, hba2+/bfr1+ and pmd1+, which encode energy-dependent transport proteins involved in multidrug resistance. Furthermore, we demonstrate that Pap1 is regulated by stress-dependent changes in subcellular localization. On imposition of oxidative stress, the Pap1 protein relocalizes from the cytoplasm to the nucleus in a process that is dependent on the Sty1 kinase. This relocalization is the result of regulated protein export, rather than import, and involves the Crm1 (exportin) nuclear export factor and the dcd1+/pim1+ gene that encodes an Ran nucleotide exchange factor.

Activating Transcription Factor 1↗
PubMed1998

Essential role of tubulin-folding cofactor D in microtubule assembly and its association with microtubules in fission yeast.

The main structural components of microtubules are alpha- and beta-tubulins. A group of proteins called cofactors are crucial in the formation of assembly-competent tubulin molecules in vitro. Whilst an in vitro role is emerging for these cofactors, their biological functions in vivo remain to be established. In order to understand the fundamental mechanisms that determine cell polarity, we have screened for fission yeast mutants with altered polarity. Here we show that alp1+ encodes a homologue of cofactor D and executes a function essential for cell viability. A temperature-sensitive alp1 mutant shows a variety of defects including abnormal mitoses, loss of microtubule structures, displacement of the nucleus, altered growth polarity and asymmetrical cell division. Overexpression of Alp1 is lethal in wild-type cells, resulting in altered cell shape, but is rescued by co-overexpression of beta-tubulin. Alp1 co-localizes with microtubules, both interphase arrays and mitotic spindles. Furthermore, Alp1 binds to and co-sediments with taxol (paclitaxel)-stabilized porcine microtubules. Our results suggest that, in addition to a function in the folding of beta-tubulin, cofactor D may play a vital role in microtubule-dependent processes as a microtubule-associated protein.

Amino Acid Sequence↗
PubMed1998

A comparative analysis of the proteins between the fibroblasts from Werner's syndrome patients and age-matched normal individuals using two-dimensional gel electrophoresis.

Werner's syndrome (WS) is an autosomal recessive disorder causing symptoms of premature aging. The fibroblasts of WS patients have a shorter life-span than normal fibroblasts. We analyzed the fibroblast proteins from three WS patients and from three age-matched normal individuals using two-dimensional gel electrophoresis and image processing. The expressions of 12 proteins were shown to be augmented or suppressed in WS fibroblasts compared with normal fibroblasts: 11 of 12 spots on the electrophoresis gel of WS fibroblasts were denser than the corresponding spots of normal individual fibroblasts, while the remaining one spot was fainter in WS fibroblasts than in normal fibroblasts. The abundance of these proteins were compared to those of the corresponding proteins from normal fibroblasts at various cell passages in vitro reported in the TMIG-2DPAGE database. The result shows that the change in the protein patterns in in vitro aging did not necessarily correspond to the change in WS fibroblasts, except for three proteins abundant in WS fibroblasts, which increased their abundance during in vitro aging. These results suggest that the premature aging process of WS fibroblasts shares only part of the in vitro aging process of normal fibroblasts.

Adult↗
PubMed1998

Regulated vacuole fusion and fission in Schizosaccharomyces pombe: an osmotic response dependent on MAP kinases.

BACKGROUND: The budding yeast Saccharomyces cerevisiae uses two mitogenactivated protein (MAP) kinase cascades, the Hog1p and the Mpk1p pathways, to signal responses to hypertonic and hypotonic stress, respectively. Mammalian cells and the fission yeast Schizosaccharomyces pombe have functional homologues of Hog1p - p38/RK/CSBP and Sty1 - which, unlike Hog1p, also mediate other responses. We have investigated the involvement of S. pombe MAP kinase pathways in signalling a newly described response to osmotic stress - that of vacuole fusion and fission. RESULTS: When S. pombe is placed into water, its vacuoles rapidly fuse into larger structures enclosing a greater proportion of the cell's volume. Under some conditions, its vacuoles can slowly fragment in response to salt. Fission requires the Sty1 pathway and also Pmk1, the homologue of S. cerevisiae Mpk1p. Fusion requires Pmk1, Ypt7 - the homologue of a protein involved in S. cerevisiae vacuole fusion - and part of the Sty1 pathway, although Sty1 phosphorylation is unaffected by hypotonic conditions. CONCLUSIONS: Vacuole fusion and fission appear to be homeostatic mechanisms that restore the concentration of the cytosol. Vacuole fusion, like stimulated secretion in higher eukaryotes, is a rapid and specific process of membrane fusion in response to an external stimulus. The Sty1 pathway, in addition to its role in responding to hypertonic stress, is required at a basal level for the expression of factors required to respond to hypotonic stress - a mechanism that may allow the cell to use a common pathway for different responses.

Amino Acid Sequence↗
PubMed1998

Effect of a 3'-->5' exonuclease with a proofreading function on the fidelity of error-prone DNA polymerase alpha from regenerating liver of aged rats.

A nuclease that releases noncomplementary nucleotides from the 3'-end of DNA was isolated and highly purified from rat liver extract. The d(T9-C) priming activities for DNA synthesis in vitro by DNA polymerases alpha and beta were recovered by the addition of this enzyme, which itself does not contain a DNA polymerase activity. This nuclease hydrolysed nucleotides from the 3'-end, but did not remove [32P]-labeled nucleotides from the 5'-terminus of specifically labeled DNA. Also, the reaction products released from the 3'-end of DNA were all mononucleotides. These results indicate that the exonuclease is a 3'-->5' exonuclease with properties the same as those of DNase VII from human placenta. Rat DNase VII requires 4 mM MgCl2 or 0.125 mM MnCl2 for maximum activity, and shows a pH optimum of 7.5. These optimal conditions are similar to those of DNA polymerases, and indicate that both rat DNase VII and DNA polymerases are able to act under same conditions. Non-complementary nucleotide incorporation by DNA polymerase alpha from aged rat has been observed during in vitro DNA synthesis on poly dA-dT10. The amount of this mis-incorporation is decreased by the coexistence of the 3'-->5' exonuclease, but not all errors are edited out. Thus, this rat DNase VII is suggested to play an important role in proofreading during DNA synthesis.

Aging↗