• Animal cells and systems
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• 제2권4호
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• pp.521-527
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• 1998

The turnover of epidermal cells after seawater adaptation of the freshwater fishwas studied in the guppy (Poecilia reticulata) by means of Proliferating cell nucleus antigen (PCNA) immunocytochemistry and transmission electron microscopy. The number of PCNA-immunoreactive cells in the epidermis of the seawater-adapted guppies, which becomes thinner than that in the fresh-water, generally increases four times as much. Degeneration of filament-containing cells by necrosis or apoptosis occurs mainly in epidermal cells. Apoptotic filament-containing cells seem to be shed into the water in the environment instead of phagocytosis by adjacent macrophages. The apoptotic chloride cell has a highly condensed cytoplasm and the lumen of tubular system is distended. The apoptotic mucous cell, which has an electron-dense cytoplasm, is characterized by the presence of a large multivesicular body of different electron densities. Macrophages contain many electron-dense lysosomal bodies and large vesicles filled with cellular debris. It is concluded that mitosis and apoptosis of epidermal cells are greatly stimulated when fish are adapting to seawater. This result reflects an increase in epidermal cell turnover by change of environmental salinity.

• Animal cells and systems
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• 제4권1호
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• pp.23-30
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• 2000

Horizontal starch gel electrophoresis for 29 populations (n=543) of the wrinkled frog, Rana rugosa, from Korea and Japan was peformed to assess the degree of genic variation and genetic diversity, and to understand the biogeographic pattern of distribution and speciation. A sum of 22 presumptive loci was screened from 17 enzymes and general proteins. Four loci, Aco, Est-3, Me-2, and Pgm, demonstrated high levels of polymorphism. The degree of average genetic variation of R. rugosa was P=22.7% (9.1-40.9%), Ho=0.086 (0.048-0.165) and He=0.090 (0.042-0.168). In the south-eastern region of the Korean peninsula (Chongsong, Yongchon, Ulsan, Kyongju, Pohang, yongdok and Ulchin), a few unique alleles in the Mpi locus were detected and their biogeographic implications were considered. The degree of genetic differentiation among the Korean populations was moderate (S=0.900), whereas the degree of genetic diversity between Korean and Japanese populations was notably high (S=0.687, D=0.293). This result corresponds with the data obtained by the mitochondrial cytochrome b gene sequence (Lee et al., 1999) suggesting that the Korean and Japanese R. rugosa might have evolved a specific level of genetic differentiation since their geographic isolation.

• Animal cells and systems
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• 제7권1호
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• pp.63-68
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• 2003

Until recently, interest in human complement receptor type I (CR1) has focused on immune complex processing, which contributed to our understanding of regulatory mechanism of complement activation. However, the promoter structure and transcriptional regulation of human CR1 gene has not been clear. To study the unique regulation of human CR1 gene expression, we assessed promoter activity of the $5^1$-flanking region of human CR1 gene using transient transfection and gel mobility shift assays. In this study we demonstrated that NF-Y binds to the inverted CCAAT element and that the functional interaction with protein(s) which bind to the GC-rich motif may be necessary for optimal transcription of human CR1 gene. We also show that sequence elements which located at-95/58 and +45/+50 are important for optimal transcription of CR1 gene.

• Molecules and Cells
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• 제41권12호
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• pp.1033-1044
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• 2018

As sessile organisms, plants have evolved to adjust their growth and development to environmental changes. It has been well documented that the crosstalk between different plant hormones plays important roles in the coordination of growth and development of the plant. Here, we describe a novel recessive mutant, mildly insensitive to ethylene (mine), which displayed insensitivity to the ethylene precursor, ACC (1-aminocyclopropane-1-carboxylic acid), in the root under the dark-grown conditions. By contrast, mine roots exhibited a normal growth response to exogenous IAA (indole-3-acetic acid). Thus, it appears that the growth responses of mine to ACC and IAA resemble those of weak ethylene insensitive (wei) mutants. To understand the molecular events underlying the crosstalk between ethylene and auxin in the root, we identified the MINE locus and found that the MINE gene encodes the pyridoxine 5′-phosphate (PNP)/pyridoxamine 5′-phosphate (PMP) oxidase, PDX3. Our results revealed that MINE/PDX3 likely plays a role in the conversion of the auxin precursor tryptophan to indole-3-pyruvic acid in the auxin biosynthesis pathway, in which TAA1 (TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS 1) and its related genes (TRYPTOPHAN AMINOTRANSFERASE RELATED 1 and 2; TAR1 and TAR2) are involved. Considering that TAA1 and TARs belong to a subgroup of PLP (pyridoxal-5′-phosphate)-dependent enzymes, we propose that PLP produced by MINE/PDX3 acts as a cofactor in TAA1/TAR-dependent auxin biosynthesis induced by ethylene, which in turn influences the crosstalk between ethylene and auxin in the Arabidopsis root.

• BMB Reports
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• 제48권5호
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• pp.239-240
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• 2015

Dysregulation of cytokine expression causes inflammatory diseases or chronic infection conditions. We have identified that Tat-activating regulatory DNA-binding protein-43 (TDP-43) is involved in cytokine RNA processing in order to promote an optimal immune response. The interaction of TDP-43 with spliceosomal components from the Cajal body leads to the formation of a novel sub-nuclear body called the Interleukin (IL)-6 and IL-10 Splicing Activating Compartment (InSAC). TDP-43 binds to the IL-6 and IL-10 RNAs in a sequence-dependent manner. In cell-based studies, we observed that lipopoly-saccharide (LPS) stimulation induces the formation of the InSAC through TDP-43 ubiquitination, thereby influencing the processing and expression levels of IL-6 RNA. Moreover, TDP-43 knockdown in vivo results in a decrease in IL-6 production and its RNA splicing and stability. Thus, these findings demonstrate that the InSAC is linked to the activation and modulation of the immune response. [BMB Reports 2015; 48(5): 239-240]

• BMB Reports
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• 제33권5호
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• pp.391-395
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• 2000

Calexcitin, a calcium-binding protein, was previously cloned and functionally characterized in the squid Loligo pealei. We now report the cloning of a second form of Calexcitin, Calexcitin-2, found in the squid Todarodes pacificus optic lobe. Calexcitin-2 has a significantly different carboxyl terminal region than Calexcitin-1. It lacks the CAAX motif, which is a farnesylation site. The amino acid sequence of Calexcitin-2 shows an 84% identity with Calexcitin-1 and also displays a strong cross immunoreactivity. Western blotting shows that Calexcitin-2 was expressed exclusively in the optic lobe region of squid, but not in other body organs. Regardless of its lack of conserved regions for GTP-binding, Calexcitin-2 shows moderately low affinity GTP-binding and also shows dramatic conformational change induced by GTP-binding. Three possible GTP-binding region mutations, K142A, D144A, and K157A, did not change the G TP binding affinity. This raises the possibility that Calexcitin-2 may have a novel GTP-binding motif.

• BMB Reports
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• 제51권1호
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• pp.5-13
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• 2018

Formation of toxic protein aggregates is a common feature and mainly contributes to the pathogenesis of neurodegenerative diseases (NDDs), which include amyotrophic lateral sclerosis (ALS), Alzheimer's, Parkinson's, Huntington's, and prion diseases. The transglutaminase 2 (TG2) gene encodes a multifunctional enzyme, displaying four types of activity, such as transamidation, GTPase, protein disulfide isomerase, and protein kinase activities. Many studies demonstrated that the calcium-dependent transamidation activity of TG2 affects the formation of insoluble and toxic amyloid aggregates that mainly consisted of NDD-related proteins. So far, many important and NDD-related substrates of TG2 have been identified, including $amlyoid-{\beta}$, tau, ${\alpha}-synuclein$, mutant huntingtin, and ALS-linked trans-activation response (TAR) DNA-binding protein 43. Recently, the formation of toxic inclusions mediated by several TG2 substrates were efficiently inhibited by TG2 inhibitors. Therefore, the development of highly specific TG2 inhibitors would be an important tool in alleviating the progression of TG2-related brain disorders. In this review, the authors discuss recent advances in TG2 biochemistry, several mechanisms of molecular regulation and pleotropic signaling functions, and the presumed role of TG2 in the progression of many NDDs.

• Molecules and Cells
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• 제37권5호
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• pp.357-364
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• 2014

Medulloblastoma, the most common malignant brain tumor in children, is a disease whose mechanisms are now beginning to be uncovered by high-throughput studies of somatic mutations, mRNA expression patterns, and epigenetic profiles of patient tumors. One emerging theme from studies that sequenced the tumor genomes of large cohorts of medulloblastoma patients is frequent mutation of RNA binding proteins. Proteins which bind multiple RNA targets can act as master regulators of gene expression at the post-transcriptional level to co-ordinate cellular processes and alter the phenotype of the cell. Identification of the target genes of RNA binding proteins may highlight essential pathways of medulloblastomagenesis that cannot be detected by study of transcriptomics alone. Furthermore, a subset of RNA binding proteins are attractive drug targets. For example, compounds that are under development as anti-viral targets due to their ability to inhibit RNA helicases could also be tested in novel approaches to medulloblastoma therapy by targeting key RNA binding proteins. In this review, we discuss a number of RNA binding proteins, including Musashi1 (MSI1), DEAD (Asp-Glu-Ala-Asp) box helicase 3 X-linked (DDX3X), DDX31, and cell division cycle and apoptosis regulator 1 (CCAR1), which play potentially critical roles in the growth and/or maintenance of medulloblastoma.

• BMB Reports
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• 제55권10호
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• pp.494-499
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• 2022

PTEN-induced putative kinase 1 (PINK1) is a serine/threonine kinase that phosphorylates several substrates and exerts neuroprotective effects against stress-induced apoptotic cell death. Mutations in PINK1 have been linked to autosomal recessive forms of Parkinson's disease (PD). Mitophagy is a type of autophagy that selectively promotes mitochondrial turnover and prevents the accumulation of dysfunctional mitochondria to maintain cellular homeostasis. Toll-interacting protein (Tollip) was initially identified as a negative regulator of IL-1β receptor signaling, suppressing inflammatory TLR signaling cascades. Recently, Tollip has been reported to play a role in autophagy and is implicated in neurodegeneration. In this study, we determined whether Tollip was functionally linked to PINK1-mediated mitophagy. Our results demonstrated that Tollip promoted the mitochondrial processing of PINK1 and altered the localization of PINK1, predominantly to the cytosol. This action was attributed to increased binding of PINK1 to mitochondrial processing peptidase β (MPPβ) and the subsequent increase in MPPβ-mediated mitochondrial PINK1 cleavage. Furthermore, Tollip suppressed mitophagy following carbonyl cyanide m-chlorophenylhydrazone-induced mitochondrial dysfunction. These findings suggest that Tollip inhibits mitophagy via the PINK1/parkin pathway upon mitochondrial damage, leading to the blockade of PINK1-mediated neuroprotection.

• Animal cells and systems
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• 제1권2호
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• pp.351-354
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• 1997

The distributions of G to A substitution ($G^{-75}{\rightarrow}A$) mutation in the human apolipoprotein A1 (APOAI) gene promoter region and glutathione S-tran-sferase Mu1 (GSTM1) gene deletion were examined in subjects with Korean population. The $G^{-75}{\rightarrow}A$ mutation of APOA1 was genotyped by the polymerase chain reaction (PCR) and subsequent digestion of the PCR product using either Mspl or Mval (n=206). The observed numbers of GG, GA and AA genotypes were 132, 63 and 11, respectively. The allele frequencies of G and A were 0.794 and 0.206, respectively. The GSTM1 gene deletion was simply examined by the PCR amplification (n=106). The observed numbers of null type ($GSTM1^*0/GSTM1^*0$) and positive type were 55 and 51, respectively. The allele frequency of $GSTM1^*0$ was 0.720.