In order to improve the removal ability of phosphate, Spheroplast fusions were performed among auxotrophic mutants of Aeromonas hydrophila isolated from waste water, named A13 and A14, Aci37 auxotrophic mutant of Acinetobactercalcoaceticus, and auxotrophic E. coli HR262/pCE27 carring pit gene. Eight fusants obtained from this experiment showed different biochemical characteristics. When the rate of phosphate uptake among fusants (F1-F8) was investigated in Phosphate Uptake Medium (PUM), F8 strain showed the highest rate for phosphate removal, 7 times as much as control after two hours incubation. The role of cations ($Mg^{++}$ ,$Ca^{++}$ , $K^{+}$ in phosphate uptade by F8 was also investigated in PUM without each salt. $K^{+}$ seemed to be crucial. Being compared with phosphate untake rate in PUM, that in PUM without $K^{+}$ was reduced 1.5 times. Therefore, by applying F8 strain and $K^{+}$ in practical environmental system, the increased efficiency in phosphate removal can be derived.
The Crustacean hyperglycemic hormone (CHH) has been shown to exist as multiple molecular forms in several crustacean species. In Penaeus monodon, a gene encoding CHH (so-called Pem-CHH1) was recently described. In this study, the molecular structures of two other CHH genes (Pem-CHH2 and Pem-CHH3) are reported. Both the Pem-CHH2 and Pem-CHH3 genes contain three exons that are separated by two introns that are similar to the structure of other genes in the same family. An analysis of the upstream nucleotide sequences of each Pem-CHH gene has identified the putative promoter element (TATA box) and putative binding sites for several transcription factors. The binding sites for CREB, Pit-1, and AP-1 were found upstream of all three Pem-CHH genes. A Southern blot analysis showed that at least one copy of each Pem-CHH gene was located within the same 10 kb genomic DNA fragment. These results suggest that the CHH genes are arranged in a cluster in the genome of P. monodon, and that their expression may be modulated by similar mechanisms.
This study was carried out to investigate the association of POU1F1 (POU domain, class 1, transcription factor 1, Pit1, renamed as POU1F1) gene with backfat thickness (mm), carcass weight (kg), pH, and color values ($L^*$, $a^*$, $b^*$) in crossbred pigs (Landrace ${\times}$ Yorkshire ${\times}$ Duroc). Frequency of the AA genotype indel was at the highest level (66.67%). Frequency of A allele (0.81) was higher than that of b allele (0.19). This population followed Hardy-Weinberg equilibrium. Carcass weights and $a^*$ values of the three genotypes were all significantly different (p < 0.05), respectively. However, backfat thickness, $L^*$, $b^*$, visual color, and pH of the three genotypes were not significantly different (p > 0.05). Visual color was negatively correlated with $L^*$ (r = -0.521) and $b^*$ (r = -0.390) values, $L^*$ value was correlated with $b^*$ (r = 0.419) value, and $a^*$ value was positively correlated with $b^*$ (r = 0.612) value. These results indicate that the POU1F1 gene affected carcass weight and meat redness.
Objective: This study investigated the effects of Hansu-Daebowon (HDW) on bone resorption in vitro and bone loss in vivo. Methods: Osteoclast differentiation was measured by counting TRAP (+) MNC formed from RAW 264.7 in the presence of RANKL. Bone pit formation was determined in an artificial bone slice loaded with RANKL-stimulated osteoclasts. To elucidate the mechanisms of the inhibitory effects of HDW on bone resorption and osteoclast differentiation, osteoclastogenic genes (i.e. TRAP, MMP-9, NFATc1, c-Fos, and Cathepsin K) were measured using real time PCR. Furthermore, bone loss was observed using micro-CT in an LPS-treated mammal model. Results: HDW inhibited the bone pit formation in vitro and inhibited bone loss in vivo. Moreover, HDW decreased the number of TRAP (+) MNCs in the presence of RANKL, and HDW inhibited the expressions of cathepsin K, MMP-9, TRAP, NFATc1, and c-Fos in the osteoclasts. Conclusion: HDW exerts inhibitory effects on bone loss and bone resorption resulting from the inhibitions of osteoclast differentiation and osteoclastogenic gene expression.
Biosynthesis and secretion of anterior pituitary hormones are under the control of specific hypothalamic stimulatory and inhibitory factors. Among them, Growth Hormone Releasing Hormone (GHRH) is the major stimulator of pituitary somatotrophs activating GH gene expression and secretion. Human GHRH is a polypeptide of 44 amino acids initially isolated from pancreatic tumors, and the gene for the hypothalamic form of GHRH is organized into 5 exons spanning over 10 kilobases (kb) on genomic DNA and encodes a messenger RNA of 700-750 nucleotides. Several neuropeptides classically associated with the hypothalamus have been found in the extrahypothalamic regions, suggesting the existence of novel sources, targets and functions. GHRH-like immunoreactivity has been found in several peripheral sites, including placenta, testis, and ovary, indicating that GHRH may also have regulatory roles in peripheral reproductive organs. Furthermore, higher molecular weight forms of the GHRH transcripts were identified from these organs (1.75 kb in testis; 1.75 and >3 kb in ovary). These tissue-specific expression of GHRH gene suggest the existence of unique regulatory mechanism of GHRH expression and function in these organs. In fact, placenta-specific and testis-specific promoters for GHRH transcripts which are located in about 10 kb upstream region of hypothalamic promoter were reported. The use of unique promoters in extrahypothalamic sites could be refered in a different control of GHRH gene and different functions of the translated products in these tissues. Somatotrophs and lactotrophs have been thought to be derived from a common bipotential progenitor, the somatolactotrophs, which give origins to either phenotypes. Although the precise mechanism responsible for the lactotroph differentiation in the anterior pituitary gland has not been yet clalified, there are several candidators for the generation of lactotrophs. In human, the presence of GHRH peptides with different size from authentic hypothalamic form in the normal anterior pituitary and several types of adenoma were demonstrated. Recently our group found the existence of immunoreactive GHRH and its transcript from the normal rat anterior pituitary (gonadotroph> somatotroph> lactotroph), and the GHRH treatment evoked the increased proliferation rate of anterior pituitary cells in vitro. The transgenic mouse models clearly shown that GHRH or NGF overexpression by anterior pituitary cells induced development of pituitary hyperplasia and adenomas particularly GH-oma and prolactinoma. Taken together, we hypothesize that the pituitary GHRH could serve not only as a modulator of hormone secretion but as a paracrine or autocrine regulator of anterior pituitary cell proliferation and differentiation. Interestingly enough, the expression of Pit-1 homeobox gene (the POU class transcription factor) was confined to somatotrophs, lactotrophs and somatolactotrophs in which GHRH receptors are expressed commonly. Concerning the mechanism of somatolactotroph and lactotroph differentiation in the anterior pituitary, we have focused following two possibilities; (1) changes in the relative levels or interactions of both hypothalamic and intrapituitary factors such as dopamine, VIP, somatostatin, NGF and GHRH; (2) alterations of GHRH-GHRH receptor signaling and Pit-1 activity may be the cause of lactotroph differentiation or pituitary hyperplasia and adenoma formation. Extensive further studies will be necessary to solve these complicated questions.
Objectives : The aim of this study was to investigate the effects of bisphenol A (BPA), an estrogen-like environmental endocrine disrupter, on the placental function and reproduction in rats. The mRNA levels of the placental prolactin-growth hormone(PRL-GH) gene family, placental trophoblast cell frequency and reproductive data were analyzed. Methods : The pregnancies of F344 Fisher rats ($160g{\pm}20g$) were detected by the presence of the copulatory plug or sperm in the vaginal smear, which marked Day 0 of pregnancy. Pregnant rats were divided into three groups. The control group was intraperitoneally injected with a sesame oil vehicle. The two remaining groups were injected with 50 or 500 mg/kg B.W/day of BPA, resuspended in sesame oil, on either days 7 to 11 or 16 to 20 of pregnancy, with the rats sacrificed on either day 11 or 20, respectively. The mRNA levels of PRL-GH and Pit-1a and b isotype genes were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction. The hormone concentrations were analyzed by radioimmunoassay, and the frequency of the placental trophoblast cells observed by a histochemical study. Reproductive data, such as the placental weight and litter size, were surveyed on day 20. The fetal weight was surveyed for 4 weeks after birth. A statistical analysis was carried out using the SAS program (version 8.1). Results : The mRNA levels of the PRL-GH gene family, such as placental lactogen I, Iv and II, prolactin like protein A, C and Cv, and decidual prolactin-related protein were significantly reduced due to BPA exposure. The mRNA levels of the Pit-1a and b isotype genes, which induce the expression of the PRL-GH gene family in the rat placenta, were also reduced due to BPA exposure. The PL-Iv and PL-II concentrations were reduced in the BPA exposed group. During the middle to last stage of pregnancy (Days 11-20), a high dose of BPA exposure reduced the frequency of spongiotrophoblast cells, which are responsible for the secretion of the PRL-GH hormones. Reproductive data, such as the placental and fetal weights and the litter size, were reduced, but that of the pregnancy period was extended in the BPA exposed compared to the control group. Conclusions : BPA disrupts the placental functions in rats, which leads to reproductive disorders.
The 13 major blast resistance(R) genes against Magnaporthe grisea were screened in a number of Korean rice varieties using molecular markers. Of the 98 rice varieties tested, 28 were found to contain the Pia gene originating from Japanese japonica rice genotypes. The Pib gene from BL1 and BL7 was incorporated into 39 Korean japonica varieties, whereas this same gene from the IRRI-bred indica varieties was detected in all Tongil-type varieties. We also found that 17 of the japonica varieties contained the Pii gene. The Pii gene in Korean rice varieties originates from the Korean japonica variety Nongbaeg, and Japanese japonica varieties Hitomebore, Inabawase, and Todorokiwase. The Pi5 gene, which clusters with Pii on chromosome 9, was identified only in Taebaeg. Thirty-four varieties were found to contain alleles of the resistance gene Pita or Pita-2. The Pita gene in japonica varieties was found to be inherited from the Japanese japonica genotype Shimokita, and the Pita-2 gene was from Fuji280 and Sadominori. Seventeen japonica and one Tongil-type varieties contained the Piz gene, which in the japonica varieties originates from Fukuhikari and 54BC-68. The Piz-t gene contained in three Tongil-type varieties was derived from IRRI-bred indica rice varieties. The Pi9(t) gene locus that is present in Korean japonica and Tongil-type varieties was not inherited from the original Pi9 gene from wild rice Oryza minuta. The Pik-multiple allele genes Pik, Pik-m, and Pik-p were identified in 24 of the varieties tested. In addition, the Pit gene inherited from the indica rice K59 strain was not found in any of the Korean japonica or Tongil-type varieties tested.
The AT motif-binding factor (ATBF1) not only interacts with protein inhibitor of activated signal transducer and activator of transcription 3 (STAT3) (PIAS3) to suppress STAT3 signaling regulating embryo early development and cell differentiation, but is required for early activation of the pituitary specific transcription factor 1 (Pit1) gene (also known as POU1F1) critically affecting mammalian growth and development. The goal of this study was to detect novel nucleotide variations and haplotypes structure of the ATBF1 gene, as well as to test their associations with growth-related traits in goats. Herein, a total of seven novel single nucleotide polymorphisms (SNPs) (SNP 1-7) within this gene were found in two well-known Chinese native goat breeds. Haplotypes structure analysis demonstrated that there were four haplotypes in Hainan black goat while seventeen haplotypes in Xinong Saanen dairy goat, and both breeds only shared one haplotype (hap1). Association testing revealed that the SNP2, SNP5, SNP6, and SNP7 loci were also found to significantly associate with growth-related traits in goats, respectively. Moreover, one diplotype in Xinong Saanen dairy goats significantly linked to growth related traits. These preliminary findings not only would extend the spectrum of genetic variations of the goat ATBF1 gene, but also would contribute to implementing marker-assisted selection in genetics and breeding in goats.
Kim, Seonyoung;Kang, Seok-Seong;Choi, Soo-Im;Kim, Gun-Hee;Imm, Jee-Young
Journal of Microbiology and Biotechnology
/
제29권1호
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pp.11-20
/
2019
Ecklonia cava, an edible marine brown alga (Laminariaceae), is a rich source of bioactive compounds such as fucoidan and phlorotannins. Ecklonia cava extract (ECE) was prepared using 70% ethanol extraction and ECE contained 67% and 10.6% of total phlorotannins and dieckol, respectively. ECE treatment significantly inhibited receptor activator of nuclear $factor-{\kappa}B$ ligand (RANKL)-induced osteoclast differentiation of RAW 264.7 cells and pit formation in bone resorption assay (p <0.05). Moreover, it suppressed RANKL-induced $NF-{\kappa}B$ and mitogen-activated protein kinase signaling in a dose dependent manner. Downregulated osteoclast-specific gene (tartrate-resistant acid phosphatase, cathepsin K, and matrix metalloproteinase-9) expression and osteoclast proliferative transcriptional factors (nuclear factor of activated T cells-1 and c-fos) confirmed ECE-mediated suppression of osteoclastogenesis. ECE treatment ($100{\mu}g/ml$) increased heme oxygenase-1 expression by 2.5-fold and decreased intercellular reactive oxygen species production during osteoclastogenesis. The effective inhibition of RANKL-stimulated osteoclast differentiation and oxidative stress by ECE suggest that ECE has therapeutic potential in alleviating osteoclast-associated disorders.
Objectives This study was performed to evaluate the effect of Pyrola japonica extract (NJ) and its principal constituent, homoarbutin (HA) on osteoclast differentiation and gene expression and bone resorption. The osteoclastogenesis and gene expression were determined in receptor activator of nuclear factor kappa B ligand (RANKL)-stimulated RAW264.7 cell. Methods In order to evaluate the effect of HA extracted from NJ on bone resorption, osteoclasts were used to be differentiated and formed by stimulating RAW264.7 cells with RANKL. Tartarate-resistant acid phosphatase (TRAP) (+) polynuclear osteoclast formation ability was evaluated, and differentiation control genes including cathepsin K, matrix metalloproteinases-9 (MMP-9), and TRAP in osteoclast differentiation were analyzed by real-time polymerase chain reaction (PCR). Immunoblotting was performed to measure the effect of mitogen-activated protein kinase (MAPK) factors on bone resorption, and the effect of osteoclasts on osteoclast differentiation was measured. Results Both NJ and high concentration of HA blocked RANKL-stimulated differentiation from RAW264.7 cell to TRAP-positive multinucleated cells. NJ reduced RANKL-induced expression of TRAP, cathepsin K. Both NJ and high concentration of HA inhibited RANKL-mediated expression of MMP-9, nuclear factor of activated T-cells, cytoplasmic 1, and cellular Jun-fos. NJ suppressed RANKL-stimulated expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase, tumor necrosis factor-alpha, and levels of interleukins. Both NJ and HA decreased bone resorption in osteoclast-induced bone pit formation model. Conclusions These results suggest that NJ and HA blocked bone resorption by decreasing RANKL-mediated osteoclastogenesis through down-regulation of genes for osteoclast differentiation.
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