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PubMed2001

Features of the two gene pairs RD-SKI2W and DOM3Z-RP1 located between complement component genes factor B and C4 at the MHC class III region.

Located at the 30 kb genomic region between complement factor B and component C4 are four ubiquitously expressed genes RD, SKI2W, DOM3Z and RP1. Besides RP1, the protein products of the other three genes each has highly conserved homologues or related proteins in lower eukaryotes, contains leucine zipper motifs for protein interaction, and plays important roles related to RNA metabolism. RD is a subunit of the negative transcription elongation factor, critical for the regulation of gene expression. It has an RNA recognition motif and 24 copies of Arg-Asp (RD) repeats. Ski2w is a nucleolar and cytoplasmic protein that has a putative RNA helicase domain. Fusion proteins of human Ski2w expressed in insect cells and bacteria have ATPase activity. The cytoplasmic protein of human Ski2w is associated with the polysomes and probably the 40S subunit of ribosomes. Ski2w is probably involved in the regulation of translation and RNA turnover. Dom3z is a nuclear protein whose yeast homologue forms a complex with an exoribonuclease. RP1 (or STK19) is a Ser/Thr nuclear protein kinase. No homologues of RP1 in lower eukaryotes have been discovered. Six polymorphic residues are present in human Ski2w and two in Dom3z. The potential roles of Ski2w and Dom3z on the clearance of degraded nuclear and cytoplasmic RNA raised their possibilities as susceptibility genes of systemic lupus erythematosus that is a disease with flawed processes in the removal of apoptotic materials.

Amino Acid Sequence↗
PubMed1989

Liver-specific and high-level expression of human serum amyloid P component gene in transgenic mice.

To analyze the regulation of human serum amyloid P component (SAP) gene expression, we have produced seven transgenic mice. The 3.3 kb human SAP genes containing about 0.8 kb of 5' and 1.5 kb of 3' flanking region were injected into fertilized eggs of C57BL/6 mice. In five of the seven transgenic mice, human SAP was detected in the sera and serum concentrations were higher than that of human serum in three lines. The human SAP gene was expressed only in the liver. Amounts of human mRNA in the liver and serum concentrations of human SAP were roughly proportional to the copy number of the integrated gene. Human SAP production lowered the serum levels of mouse endogenous SAP. With the intraperitoneal administration of lipopolysaccharide, the mRNA levels in the liver and serum levels of mouse SAP increased several-fold in both the control and transgenic mice. On the other hand, neither the mRNA nor the serum levels of human SAP increased significantly.

Animals↗
PubMed1994

Phylogeny of the C3/C4/C5 complement-component gene family indicates that C5 diverged first.

A phylogenetic analysis of DNA sequences from the C3/C4/C5 complement-component family of vertebrates supported the hypothesis that the C5 gene diverged first from the common ancestor of C3 and C4 and that C3 and C4 diverged later. The close relationship of C3 and C4 was further supported by the fact that a hagfish complement-component gene showed evidence of being more closely related to both C3 and C4 than to C5. This phylogeny is most consistent with the hypothesis that the alternative complement pathway was the first to evolve, followed by the terminal pathway and then by the classical pathway.

Animals↗
PubMed1990

Mapping and conservation of the group-specific component gene in mouse.

The group-specific component (GC), also known as the vitamin D-binding protein, transports vitamin D and its metabolites in plasma to target tissues throughout the body. The GC gene shares an evolutionary origin with genes encoding albumin (ALB) and alpha-fetoprotein (AFP). All three genes are descendants of an evolutionary ancestor that arose from an intragenic triplication. As a result, each gene is composed of three homologous domains. The study described here characterizes and compares mouse GC to the corresponding nucleotide and amino acid sequences of GC from human and rat. The deduced amino acid sequence of mouse GC was 78% identical to human and 91% identical to rat GC. The results suggest that, unlike the corresponding sequences in the ALB and AFP genes, chromosomal sequences encoding the first domain and the leader sequence of the GC gene have specifically been conserved throughout vertebrate evolution. Protection of domain I during evolution may correlate with an important functional aspect of its sequence. The mouse GC gene was mapped to chromosome 5, where the ALB and AFP genes are also located, demonstrating conservation of the three genes in vertebrate species.

Albumins↗
PubMed1988

Structure of the mouse serum amyloid P component gene.

A genomic DNA clone corresponding to the mouse serum amyloid P component (SAP) has been isolated and characterized for the first time. The numbers of exons, the relative sites of intron/exon junctions, and the size of the coding region for mature SAP protein are all in complete agreement with those of the human SAP gene. In the 5'-flanking region of the mouse SAP gene, there is a small DNA segment (43-base pairs) which is highly homologous with the corresponding region of the human SAP gene. However, most parts of the 5'-flanking regions are not conserved between the mouse and human SAP genes, and several phorbol ester-responsive element-like sequences are present only in the mouse SAP gene.

Amino Acid Sequence↗
PubMed1999

Androgen specificity of a response unit upstream of the human secretory component gene is mediated by differential receptor binding to an essential androgen response element.

The expression of secretory component (SC), the epithelial receptor for poly-immunoglobulins, is regulated in a highly tissue-specific manner. In several tissues, e.g. lacrimal gland and prostate, SC synthesis is enhanced by androgens at the transcriptional level. In this study, we describe the presence of an androgen response unit, located 3.3 kb upstream of the sc transcription initiation site and containing several 5'-TGTTCT-3'-like motifs. Although each of these elements is implicated in the enhancer function, one element, the ARE1.2 motif, is found to be the main interaction site for the androgen receptor as demonstrated in in vitro binding assays as well as in transient transfection assays. A high-affinity binding site for nuclear factor I, adjacent to this ARE, is also involved in the correct functioning of the sc upstream enhancer. The ARE1.2 motif consists of an imperfect direct repeat of two core binding elements with a three-nucleotide spacer and therefore constitutes a nonconventional ARE. We demonstrate that this element displays selectivity for the androgen receptor as opposed to glucocorticoid receptor both in in vitro binding assays and in transfection experiments. Mutational analysis suggests that the direct nature of the half-site repeat is responsible for this selectivity. We have thus determined a complex and androgen-specific response unit in the far upstream region of the human SC gene, which we believe to be involved in its androgen responsiveness in epithelial cells of different organs such as prostate and lacrimal gland. We were also able to demonstrate that the primary sequence of a single nonconventional ARE motif within the enhancer is responsible for its androgen specificity.

Androgens↗
PubMed1997

Amyloid deposition is delayed in mice with targeted deletion of the serum amyloid P component gene.

The tissue amyloid deposits that characterize systemic amyloidosis, Alzheimer's disease and the transmissible spongiform encephalopathies always contain serum amyloid P component (SAP) bound to the amyloid fibrils. We have previously proposed that this normal plasma protein may contribute to amyloidogenesis by stabilizing the deposits. Here we show that the induction of reactive amyloidosis is retarded in mice with targeted deletion of the SAP gene. This first demonstration of the participation of SAP in pathogenesis of amyloidosis in vivo confirms that inhibition of SAP binding to amyloid fibrils is an attractive therapeutic target in a range of serious human diseases.

Amyloid↗
PubMed1991

Modulation of basement membrane component gene expression in glomeruli of aminonucleoside nephrosis.

The present studies were designed to analyze mRNA levels of basement membrane components including collagen IV, laminin, and heparan sulfate proteoglycan (HSPG) in the course of puromycin aminonucleoside (PAN) nephrosis. mRNA levels for alpha 1 (IV) chain; laminin A, B1, and B2 chains; and HSPG were measured in glomeruli of PAN nephrotic rats 0, 2, 8, 14, and 20 days after PAN injection. In the nephrotic stage of PAN nephrosis (on the 8th day), mRNA levels for alpha 1 (IV) chain and laminin A, B1, and B2 chains increased, whereas those for HSPG decreased. The anionic sites in glomerular basement membrane stained by polyethyleneimine were smaller in size and fewer in number in PAN nephrotic rats than they were in control rats. In the remission stage of PAN nephrosis (on the 20th day), however, mRNA levels for alpha 1 (IV) chain and laminin A, B1, and B2 chains decreased, whereas mRNA levels for HSPG increased. Polyethyleneimine aggregates in this stage appeared to be larger and more intense than those in the nephrotic stage. These results indicate that the expression of basement membrane genes for alpha 1 (IV), laminin, and HSPG was abnormally regulated in PAN nephrosis and that this abnormal gene regulation might contribute to the development of proteinuria.

Animals↗
PubMed2001

Source and component genes of a 6-200 Mb gene cluster in the house mouse.

We identified and analyzed the genes Sp100, Csprs, and Ifi75 in two members of the genus Mus, M. musculus and M. caroli. Sp100 is a nuclear dot gene; Csprs and Ifi75 are novel genes encoding a putative G-protein coupled receptor (GPCR) and a putative transcriptional coactivator, respectively. A fourth gene, Sp100-rs, occurs in M. musculus, but not in M. caroli. Sp100-rs is a chimeric gene which arose by fusion of Sp100 and Csprs copies. Sp100-rs and Ifi75 are components of a repeat cluster that extends over 6-200 Mb of the M. musculus genome. The Sp100-rs fusion gene arose only 1-2 million years ago and has become fixed and amplified in M. musculus. Although the gene is transcribed, it appears to have no function. The repeat cluster may have become fixed in the species as a 'hitchhiker' in a 'selective sweep'.

Animals↗
PubMed2003

Molecular basis of constitutive production of basement membrane components. Gene expression profiles of Engelbreth-Holm-Swarm tumor and F9 embryonal carcinoma cells.

Engelbreth-Holm-Swarm (EHS) tumors produce large amounts of basement membrane (BM) components that are widely used as cell culture substrates mimicking BM functions. To delineate the tissue/organ origin of the tumor and the mechanisms operating in the BM overproduction, a genome-wide expression profile of EHS tumor was analyzed using RIKEN cDNA microarrays containing approximately 40,000 mouse cDNA clones. Expression profiles of F9 embryonal carcinoma cells that produce laminin-1 and other BM components upon differentiation into parietal endoderm-like cells (designated F9-PE) were also analyzed. Hierarchical clustering analysis showed that the gene expression profiles of EHS and F9-PE were the most similar among 49 mouse tissues/organs in the RIKEN Expression Array Database, suggesting that EHS tumor is parietal endoderm-derived. Quantitative PCR analysis confirmed that not only BM components but also the machineries required for efficient production of BM components, such as enzymes involved in post-translational modification and molecular chaperones, were highly expressed in both EHS and F9-PE. Pairs of similar transcription factor isoforms, such as Gata4/Gata6, Sox7/Sox17, and Cited1/Cited2, were also highly expressed in both EHS tumor and F9-PE. Time course analysis of F9 differentiation showed that up-regulation of the transcription factors was associated with those of BM components, suggesting their involvement in parietal endoderm specification and overproduction of the BM components.

Animals↗
PubMed1999

Genetic evidence for interaction between components of the yeast 26S proteasome: combination of a mutation in RPN12 (a lid component gene) with mutations in RPT1 (an ATPase gene) causes synthetic lethality.

The 19S regulatory particle of the yeast 26S proteasome consists of six related ATPases (Rpt proteins) and at least 11 non-ATPase proteins (Rpn proteins). RPN12 (formerly NIN1) encodes an Rpn component of the 19S regulatory particle and is essential for growth. To determine which subunit(s) of the 26S proteasome interact(s) with Rpn12, we attempted to screen for mutations that cause synthetic lethality in the presence of the rpn12-1 (formerly nin1-1) mutation. Among the candidates recovered was a new allele of RPT1 (formerly CIM5). This mutant allele was designated rpt1-2; on its own this mutation caused no phenotypic change, whereas the rpn12-1 rpt1-2 double mutant was lethal, suggesting a strong interaction between Rpn12 and Rpt1. The site of the rpt1-2 mutation was determined by DNA sequencing of the RPT1 locus retrieved from the mutant, and a single nucleotide alteration was found. This changes amino acid 446 of the RPT1 product from alanine to valine. The alanine residue is conserved in all Rpt proteins, except Rpt5, but no function has yet been assigned to the region that contains it. We propose that this region is necessary for Rpt1 to interact with Rpn12. The terminal phenotype of the rpn12-1 rpt1-2 double mutant was not cell cycle specific, suggesting that in the double mutant cells the function of the 26S proteasome is completely eliminated, thereby inducing multiple defects in cellular functions.

Adenosine Triphosphatases↗
PubMed2000

Segregation analysis of asthma: recessive major gene component for asthma in relation to history of atopic diseases.

Although asthma has a significant heritable component, the mode of inheritance remains controversial because of the complexity of the disease and the influence of environmental factors. Segregation analysis for asthma are performed with and without a history of atopic diseases (dermatitis and rhinitis) after adjusting for environmental factors. To investigate whether asthma may be inherited through a major gene with two alleles, the REGD program of the Statistical Analysis for Genetic Epidemiology (SAGE) package was conducted in 1,990 individuals from 227 families with at least one asthmatic child in a cross-sectional study of respiratory diseases in Southern Taiwan. Other covariates adjusted for included age, sex, current smoking, and environmental tobacco smoking. The hypothesis of Mendelian model and no parent-offspring transmission was rejected. However, when the variables of atopic disease and environmental factors were included in the model as covariates, the models for a two-allele gene with a recessive or codominant inheritance could not be rejected, and Akaike's Information Criterion was smaller (1,377. 13) for the recessive model than all of the other models tested, assuming a major gene with a population frequency of 0.56 +/- 0.04. However, Mendelian model without family effect was rejected. In conclusion, a history of asthma in parents is a strong risk factor for asthma in offspring. Under the assumptions of the applied segregation, at least one major gene exists that could be a gene involved also in allergy. However, the data suggest that a single locus gene explains a portion of asthma that is related to the history of atopic diseases. In addition, a polygenic/multifactorial (genetic and environmental factors) influence with a recessive component inheritance may be involved in the pathogenesis of asthma.

Adolescent↗
PubMed1999

Interleukin-4 and interferon-gamma synergistically increase secretory component gene expression, but are additive in stimulating secretory immunoglobulin A release by Calu-3 airway epithelial cells.

Interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) synergize to express polymeric immunoglobulin receptor (pIgR) but their combined effect, and that of IL-4 alone, on secretory immunoglobulin A (sIgA) release is unknown. Recently, we have developed an airway epithelial cell model that allows assessment of the integrated effect of a stimulus on pIgR gene and protein expression and sIgA release. With this model we show here that IL-4 and IFN-gamma dose-dependently increased pIgR mRNA and protein expression, and sIgA release. IFN-gamma and IL-4 induced similar maximal expression of pIgR, but IFN-gamma enhanced sIgA release more than IL-4. When added together, IL-4 and IFN-gamma synergistically increased pIgR mRNA and protein expression, but sIgA release was stimulated in an additive manner. Thus, IL-4 and IFN-gamma may be implicated in the increase of sIgA levels as found in mucosal inflammatory diseases. In addition, our results indicate that transport and release of empty pIgR is subject to regulatory mechanisms different from those of pIgR with bound dimeric IgA.

Cell Culture Techniques↗
PubMed1994

Pseudomonas aeruginosa possesses homologues of mammalian phenylalanine hydroxylase and 4 alpha-carbinolamine dehydratase/DCoH as part of a three-component gene cluster.

Pseudomonas aeruginosa possesses a multigene operon that includes phenylalanine hydroxylase (PhhA; phenylalanine 4-monooxygenase, EC 1.14.16.1). phhA encodes PhhA (M(r) = 30,288), phhB (M(r) = 13,333) encodes a homologue of mammalian 4 alpha-carbinolamine dehydratase/homeodomain protein transregulator, and phhC encodes an aromatic aminotransferase (M(r) = 43,237). The reading frames specifying phhB and phhC overlap by 2 bases. The P. aeruginosa PhhA appears to contain iron and is pterin dependent. Unlike the multimeric mammalian hydroxylase, the native P. aeruginosa enzyme is a monomer. The P. aeruginosa PhhA is homologous with mammalian PhhA, tryptophan hydroxylase, and tyrosine hydroxylase. Expression of PhhA from its native promoter required phhB. This may suggest a positive regulatory role for phhB, consistent with the dual catalytic and regulatory roles of the corresponding mammalian homologue.

Amino Acid Sequence↗