Life history characteristics of the protogynous parrotfish Calotomus japonicus from northwest Kyushu, Japan

In this study, we examined the life history characteristics of the parrotfish Calotomus japonicus, using individuals collected between May 2003 and May 2008 off the Nagasaki Peninsula in northwest Kyushu, Japan. Age determinations were performed using scales. Marginal increment analysis revealed that growth rings were formed annually around July. Growth in both sexes was fitted to the von Bertalanffy growth function (L _∞ = 513, k = 0.28, t ₀ = 0.03, where L _∞ is the theoretical asymptotic total length in mm, k is the growth rate coefficient and t ₀ is the theoretical time at zero length). Observed maximum age for both sexes was 8 years. We also characterized the reproductive biology of this species based on a gonadosomatic index and histological examinations of the gonads. The spawning season extends from July to October, with peak spawning activity occurring during July and August. Fish reach sexual maturity by the second year of life. Females are assumed to be multiple spawners, since we observed specimens with postovulatory follicles in ovaries containing either yolk globule oocytes or migratory nucleus oocytes. All males had secondary testes, which were characterized by the presence of an ovarian lumen structure and sperm sinuses in the gonadal wall. This indicates that all males, irrespective of whether they were initial or terminal phase males, had undergone a sexual transition. Sex change appears to occur during the spawning season, and thereafter sex-changed males are able to fertilize female eggs throughout the remainder of the current spawning season.     

Studies on endoreduplication. III. Endoreduplication induced by mitomycin C in PHA-stimulated tonsillar lymphocyte cultures

The activity of mitomycin C (MMC) to induce endoreduplication was examined in PHA-stimulated tonsillar lymphocyte cultures. Cellular kinetics of both diploid and endoreduplicated cells was studied by the combined techniques of thymidine and BrdU incorporation. The kinetic data showed that the increase of endoreduplicated cells induced by MMC correlated with the increase of the second-generation diploid cells. Also, it showed that the majority of endoreduplicated cells found at the time when the maximal number of endoreduplicated cells was obtained had incorporated BrdU only once into their diplochromosomes. This suggests that MMC-induced endoreduplicated cells originate from MMC-induced G2-arrested cells.     

In vitro promoting activity of human interferon β production by extracts of marine algae from Japan

Two hundreds species of marine algae were investigated for in vitro promoting activity of human interferon β (IFN-β) production by poly(I:C)-induced human osteosarcoma cell line, MG-63. A brown alga, Sargassum hemipyllum promoted most its activity, showing more than 11-fold. When we attempted to partially purify the active substances by particular two-step chromatography, two peaks of active fractions were obtained. These fractioned materials exhibited the heat-stable and non-cytotoxic characters with the molecular weight less than 3000. This revised version was published online in June 2006 with corrections to the Cover Date.     

Morphological Observations and Qualitative and Quantitative Studies of Auxins after Induction of Tobacco Genetic Tumor

When stem segments of tobacco F₁(Nicotiana glaucaxN. langsdorffii)seedlings were cultured on a hormone-free medium in the light,tumorous tissues were induced on the segments within 5 days.The fresh weight of the tissues increased rapidly, with a 10-foldincrease in weight every 6 days. Morphological observationsrevealed the active division of cells and the primordium-likestructures of the teratomas that had been induced during the5 days after cutting of the stem segments. In the light-growntissues of genetic tumors, IAA was revealed to be the predominantauxin by analysis by gas chromatography-mass spectrometry. NormalF₁ seedlings grown in the light contained endogenous IAA ata concentration of 3.4 ng/g fr wt. Five days after cutting,the level of endogenous IAA in stem segments rose to 96 ng/gfr wt or more, and then it decreased to 9.1 ng/g fr wt by 11days. This surge in the endogenous level of IAA may play animportant role in the induction of tobacco genetic tumor. (Received March 30, 1988; Accepted October 31, 1988)     

Selective induction of DeltaFosB in the brain after transient forebrain ischemia accompanied by an increased expression of galectin-1, and the implication of DeltaFosB and galectin-1 in neuroprotection and neurogenesis

Transient forebrain ischemia causes selective induction of DeltaFosB, an AP-1 (activator protein-1) subunit, in cells within the ventricle wall or those in the dentate gyrus in the rat brain prior to neurogenesis, followed by induction of nestin, a marker for neuronal precursor cells, or galectin-1, a beta-galactoside sugar-binding lectin. The adenovirus-mediated expression of FosB or DeltaFosB induced expression of nestin, glial fibrillary acidic protein and galectin-1 in rat embryonic cortical cells. DeltaFosB-expressing cells exhibited a significantly higher survival and proliferation after the withdrawal of B27 supplement than the control or FosB-expressing cells. The decline in the DeltaFosB expression in the survivors enhanced the MAP2 expression. The expression of DeltaFosB in cells within the ventricle wall of the rat brain also resulted in an elevated expression of nestin. We therefore conclude that DeltaFosB can promote the proliferation of quiescent neuronal precursor cells, thus enhancing neurogenesis after transient forebrain ischemia.     

shk1-D, a dwarf Arabidopsis mutant caused by activation of the CYP72C1 gene, has altered brassinosteroid levels

Brassinosteroids (BRs) are plant steroidal hormones that regulate plant growth and development. An Arabidopsis dwarf mutant, shrink1-D (shk1-D), was isolated and the phenotype was shown to be caused by activation of the CYP72C1 gene. CYP72C1 is a member of the cytochrome P450 monooxygenase gene family similar to BAS1/CYP734A1 that regulates BR inactivation. shk1-D has short hypocotyls in both light and dark, and short petioles and siliques. The seeds are also shortened along the longitudinal axis indicating CYP72C1 controls cell elongation. The expression of CPD, TCH4 and BAS1 were altered in CYP72C1 overexpression transgenic lines and endogenous levels of castasterone, 6-deoxocastasterone and 6-deoxotyphasterol were also altered. Unlike BAS1/CYP734A1 the expression of CYP72C1 was not changed by application of exogenous brassinolide. We propose that CYP72C1 controls BR homeostasis by modulating the concentration of BRs.     

Thymidine phosphorylase inhibits apoptosis induced by cisplatin

An angiogenic factor, platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP), stimulates the chemotaxis of endothelial cells and confers resistance to apoptosis induced by hypoxia. 2-Deoxy-D-ribose, a degradation product of thymidine generated by TP, partially prevents hypoxia-induced apoptosis. TP is expressed at higher levels in tumor tissues compared to the adjacent non-neoplastic tissues in a variety of human carcinomas. High expression of TP is associated with an unfavorable prognosis. To investigate the effect of TP on cisplatin-induced apoptosis, human leukemia Jurkat cells were transfected with wild-type or mutant (L148R) TP cDNA. TP inhibited a number of steps in the cisplatin-induced apoptotic pathway, activation of caspases 3 and 9 and mitochondrial cytochrome c release. These findings suggest a mechanism by which TP confers resistance to apoptosis induced by cisplatin. Moreover, mutant TP that has no enzymatic activity also suppressed cisplatin-induced apoptosis. These findings indicate that TP has cytoprotective functions against cytotoxic agents which are independent of its enzymatic activity.     

Evidence of both extra- and intracellular cysteine targets of protein modification for activation of RET kinase

By use of a specifically sulfhydryl group-reactive chemical, 1,4-butanediyl-bismethanethiosulfonate (BMTS), we studied the localization of oxidative stress-responsive target cysteines for activation of a receptor-type protein tyrosine kinase, c-RET. The chemical, which reacted with RET proteins on the cell surface for sulfhydryl-linked aggregation, induced autophosphorylation and activation of RET kinase. When extracellular domain-deleted RET mutant (RET-PTC-1) cells were exposed to BMTS, neither the molecular status nor the activity of the enzyme was affected, suggesting that the target cysteines of BMTS to which cells were exposed for reaction are located in the cysteine-rich region of the extracellular domain of RET kinase. Despite this result, the exposure of a subcellular form of c-RET or RET-PTC-1 kinase isolated by immunoprecipitation to BMTS did induce activation of the enzyme. These results suggest that cysteines in both the extracellular and the intracellular domains of RET can work as target sites of accessible BMTS and possibly other oxidative elements for structural modification and activation of RET kinase.