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Biomedical subjects

Yi Sun

Publications and source records attributed to Yi Sun.

At least 55 records · Page 3Linked to original sources
PubMed2006

[Meta-analysis of association of deletion allele of angiotensin-converting enzyme gene with coronary heart disease in China].

OBJECTIVE: To qualitatively and quantitatively assess the evidence regarding the relation of ACE I/D polymorphism to coronary heart disease (CHD) risk. METHODS: Medline (January 1994 to February 2005) and China Hospital Knowledge Databases (January 1994 to May 2005) were retrieved for all publications relating to case-control studies reporting a link between CHD risk factors and the ACE I/D polymorphism. All 16 association studies were identified and a meta-analysis was conducted by using the RevMan 4.2 estimate for odds ratio (OR) to determine whether the DD genotype might predict the outcome in CHD. RESULTS: Sixteen out of 48 identified studies reporting data on 1345 CHD patients and 1286 matched controls fulfilled these inclusion criteria. The overall distribution of genotypes in the control subjects was 35.88% II, 40.86% ID, and 23.26% DD. The odds ratio for CHD for DD versus ID/II genotypes across all studies was 2.56 [95% CI, 2.09 - 3.13]. The relative CHD risk appeared to be increased with the D allele (chi(Trend)(2) = 97.12, P < 0.01). CONCLUSIONS: ACE gene I/D polymorphism should be associated with susceptivity of coronary heart disease in China. The CHD risk is increased significantly in individuals with DD genotypes. The ACE D allele should be a risk factor for CHD.

Alleles↗
PubMed2005

A small molecule Smac-mimic compound induces apoptosis and sensitizes TRAIL- and etoposide-induced apoptosis in breast cancer cells.

Inhibitor of apoptosis protein (IAP) suppresses apoptosis through binding and inhibiting active caspases-3, -7 and -9 via its baculoviral IAP repeat (BIR) domains. During apoptosis the caspase inhibition by IAPs can be negatively regulated by a mitochondrial protein second mitochondrial-derived activator of caspase (Smac). Smac physically interacts with multiple IAPs and relieves their inhibitory effect on caspases-3, -7 and -9. Recently, a small molecule Smac-mimic compound (Smac-mimic), which potentiates TNF-related apoptosis-inducing ligand (TRAIL) and tumor necrosis factor (TNF)-alpha mediated cell death in glioblastoma T98G cells and HeLa cells, was identified and characterized. To determine the efficacy of this compound in breast cancer cells, we first measured protein expression of three IAPs: XIAP, cIAP-1, and cIAP-2 in nine independent breast cancer cell lines. Three cell lines were chosen: a high IAPs expressing line MDA-MB-231, and two low IAPs expressing lines, T47D and MDA-MB-453. The cell lines were tested for their sensitivity to Smac-mimic alone or in combination with TRAIL or etoposide. Acting alone, Smac-mimic was quite potent with a cytotoxic IC50 of 3.8 nM in high IAPs expressing MDA-MB-231 cells, but was inactive at a much higher concentration in low IAPs expressing T47D and MDA-MB-453 cells. In fact, as low as 2.5 nM of Smac-mimic alone was sufficient to activate caspase-3 and induce apoptosis in MDA-MB-231 cells. In combinational treatments with TRAIL or etoposide, Smac-mimic significantly sensitized cells to growth suppression in MDA-MB-231 cells, but to a lesser extent in T47D and MDA-MB-453 cells. Furthermore, it significantly synergized MDA-MB-231, but not T47D cells to apoptosis induced by either TRAIL or etoposide. Thus, in these cell lines, Smac-mimic acts in an apparent IAPs dependent manner to induce apoptosis alone as well as sensitizes breast cancer cells to TRAIL or etoposide induced apoptosis via caspase-3 activation.

Antineoplastic Agents, Phytogenic↗
PubMed2005

Reversal of hypermethylation and reactivation of p16INK4a, RARbeta, and MGMT genes by genistein and other isoflavones from soy.

PURPOSE: We have previously shown the reactivation of some methylation-silenced genes in cancer cells by (-)-epigallocatechin-3-gallate, the major polyphenol from green tea. To determine whether other polyphenolic compounds have similar activities, we studied the effects of soy isoflavones on DNA methylation. EXPERIMENTAL DESIGN: Enzyme assay was used to determine the inhibitory effect of genistein on DNA methyltransferase activity in nuclear extracts and purified recombinant enzyme. Methylation-specific PCR and quantitative real-time PCR were employed to examine the DNA methylation and gene expression status of retinoic acid receptor beta (RARbeta), p16INK4a, and O6-methylguanine methyltransferase (MGMT) in KYSE 510 esophageal squamous cell carcinoma cells treated with genistein alone or in combination with trichostatin, sulforaphane, or 2'-deoxy-5-aza-cytidine (5-aza-dCyd). RESULTS: Genistein (2-20 micromol/L) reversed DNA hypermethylation and reactivated RARbeta, p16INK4a, and MGMT in KYSE 510 cells. Genistein also inhibited cell growth at these concentrations. Reversal of DNA hypermethylation and reactivation of RARbeta by genistein were also observed in KYSE 150 cells and prostate cancer LNCaP and PC3 cells. Genistein (20-50 micromol/L) dose-dependently inhibited DNA methyltransferase activity, showing substrate- and methyl donor-dependent inhibition. Biochanin A and daidzein were less effective in inhibiting DNA methyltransferase activity, in reactivating RARbeta, and in inhibiting cancer cell growth. In combination with trichostatin, sulforaphane, or 5-aza-dCyd, genistein enhanced reactivation of these genes and inhibition of cell growth. CONCLUSIONS: These results indicate that genistein and related soy isoflavones reactivate methylation-silenced genes, partially through a direct inhibition of DNA methyltransferase, which may contribute to the chemopreventive activity of dietary isoflavones.

Anticarcinogenic Agents↗
PubMed2005

[Clinical evaluation of BTAstat, NMP22, HA, survivin, CD44v6, vEGF and VUC in bladder cancer diagnosis].

OBJECTIVE: To evaluate the sensitivity and specificity of BTAstat, NMP22, HA, Survivin, CD44v6, VEGF, and VUC in detection of bladder cancer. METHODS: We detect VUC, BTAstat, NMP22, HA, Survivin, CD44v6, VEGF in the urine of 10 normal case (healthy volunteers), 11 benign urological diseases patients and 52 bladder cancer patients. The sensitivity, specificity the coefficient of variation, the examining time duration and the checking costs of each marker and combined markers were assessed to evaluate the clinical value. RESULTS: There is a significant difference between the cancer group and the two control groups. The overall sensitivity and specificity of urinary tumor markers were: 42.3% and 100% for VUC; 78.8% and 90.5% for BTAstat; 76.9% and 81.0% for NMP22; 86.5% and 90.5% for HA; 67.3% and 85.7% for Survivin; 50.5% and 85.7% for CD44 and 69.2% and 95.2% for VEGF. The highest sensitivity of combined markers was 96.2% for NMP22 + HA and HA + CD44v6, whereas the lowest sensitivity of combined markers was 67.3% for VUC + CD44v6. The highest specificity (95.2%) was the combined use of VUC + NMP22 and combined use of VUC + VEGF, whereas, method that achieved the lowest specificity (66.7%) was the combined use of HA + Survivin. The most convenient examining method was the detection for BTAstat; the lowest cost examining method was the detection for HA; methods which had the best repeatability were the detection for BTAstat and urine cytology examination. CONCLUSION: Each marker had achieved its obvious clinical value in diagnosis of bladder cancer. The sensitivity of all the markers was increased with the progression of tumor grades and clinical stages, except the CD44v6. The combined use of BATstat and HA is the best examining method concerning sensitivity, specificity, feasibility and cost in each different method.

Adult↗
PubMed2005

Possible role of direct Rac1-Rab7 interaction in ruffled border formation of osteoclasts.

Rab7 has been shown to regulate the late steps of the endocytic pathway. In bone-resorbing osteoclasts, it is involved in formation of the ruffled border, which is a late endosomal-like compartment in the plasma membrane. Here we report a new Rab7-interacting protein, Rac1, another small GTPase protein that binds to the GTP-form of Rab7 as found with a two-hybrid system. We demonstrate further that Rab7 colocalizes with Rac1 at the fusion zone of the ruffled border in bone-resorbing osteoclasts. In other cell types, such as fibroblast-like cells, partial colocalization is perinuclear. Because Rac1 is known to control the actin cytoskeleton through its effectors, the Rab7-Rac1 interaction may mediate late endosomal transport between microtubules and microfilaments enabling endosomal vesicles to switch tracks and may thus also regulate ruffled border formation in osteoclasts.

Actins↗
PubMed2005

Novel insect resistance in Brassica napus developed by transformation of chitinase and scorpion toxin genes.

Transgenic plants with introduced pest-resistant gene offer an efficient alternative insect control. The novel insect-resistant gene combination, chitinase(chi) and BmkIT(Bmk), containing an insect-specific chitinase gene and a scorpion insect toxin gene was introduced into Brassica napus cultivar via Agrobacterium-mediated transformation. Fifty-seven regenerated plantlets with kanamycin-resistance were obtained. Transgenic plants were verified by Southern blot analysis. Enzyme-linked immunosorbent assay (ELISA) and bioassay of artificial inoculation with diamondback moth (Plutella maculipenis) (DBM) larvae indicated that some of the transgenic plants were high-level expression for both chitinase and scorpion toxin proteins and performed high resistance against the tested pest infestation. The genetic analysis of T(1) progeny confirmed that the inheritance of introduced genes followed the Mendelian rules.

Animals↗
PubMed2005

Role of fibrinogen-like protein 2 prothrombinase/fibroleukin in experimental and human allograft rejection.

Immune coagulation is a major contributor to the pathogenesis of xenograft rejection, viral-induced hepatocellular injury and cytokine-induced fetal loss syndrome. In this study, we investigated the contribution of the novel gene product, fibrinogen-like protein 2 (fgl2) prothrombinase, in mediating immune injury in experimental and human acute allograft rejection. Using a mouse heterotopic cardiac transplant model, mouse fgl2(mfgl2)/fibroleukin mRNA transcripts and protein were highly expressed in macrophages, CD4- and CD8-positive T lymphocytes, and endothelial cells in rejecting cardiac allografts in association with deposits of fibrin. Although mfgl2-deficient mice rejected allografts at similar rates to littermate controls, survival of grafts from mfgl2-deficient mice were prolonged and deposition of intravascular fibrin was diminished. Treatment of wild-type mice with a neutralizing anti-fgl2 Ab ameliorated histological evidence for allorejection and intravascular fibrin deposition, and resulted in an increase in graft survival. To address further the relevance of fgl2 in acute allograft rejection, we examined kidney biopsies from patients who had undergone renal transplantation. Human fgl2 mRNA transcripts and protein were markedly expressed mainly in renal tubule cells, infiltrating lymphoid cells including macrophages, CD8(+) T cells, mature B cells (plasma cells), and endothelial cells. Dual staining showed fibrin deposition was localized mainly to blood vessels, in the glomerulus and interstitium and the lumen of tubules, and occurred in association with human fgl2 expression. These data collectively suggest that fgl2 accounts for the fibrin deposition seen in both experimental and human allograft rejection and provide a rationale for targeting fgl2 as adjunctive therapy to treat allograft rejection.

Adult↗
PubMed2005

Smad4 inhibits tumor growth by inducing apoptosis in estrogen receptor-alpha-positive breast cancer cells.

Estrogen is a mitogen in most estrogen receptor-alpha (ERalpha)-positive breast cancers. We have found that Smad4, a common signal transducer in the transforming growth factor-beta superfamily, acts as an ERalpha transcriptional corepressor. Here, we show that Smad4 induces apoptosis in ERalpha-positive MCF-7 breast cancer cells, but not in ERalpha-negative MDA-MB-231 cells. Smad4 induced expression of short Bim isoforms (by alternative splicing) and Bax and release of cytochrome c in ERalpha-positive cells only, and expression of these apoptotic marker genes was reduced when ERalpha small interfering RNA was introduced. Notably, Smad4 was able to induce apoptosis in MDA-231 cells with acquired ERalpha expression. Furthermore, Smad4 inhibited ERalpha-positive tumor growth by inducing apoptosis in tumor xenografts in nude mice. The sizes of tumors expressing Smad4 were only one-tenth the size of those expressing green fluorescent protein, whereas in ERalpha-negative cells, Smad4 did not reduce the tumor size. Notably, Smad4 also promoted short Bim isoform and Bax expression and release of cytochrome c only in ERalpha-positive MCF-7 tumor xenografts. Bim was sufficient for induction of apoptosis, and the short form was the most potent inducer. Our results demonstrate that Smad4 induces apoptosis by regulating Bim splicing as an initial intrinsic signal in ERalpha-positive cells. Smad4-induced apoptosis in ERalpha-positive breast cancer cells may explain the invasive nature of ERalpha-negative breast tumors, thereby providing a potential target for breast cancer intervention.

Alternative Splicing↗
PubMed2005

Effect of hepatitis C virus nonstructural protein NS3 on proliferation and MAPK phosphorylation of normal hepatocyte line.

AIM: To study the effect of hepatitis C virus nonstructural region 3 (HCV NS3) protein on proliferation and transformation of normal human liver cell line. METHODS: QSG7701 cells were transfected with pRcHCNS3-5', pRcHCNS3-3' and pRcCMV using lipofectamine transfecting technique and selected with G418 method. Expression of HCV NS3 protein was determined by immunohistochemistry. Biologic characteristics of transfected cells were evaluated by population doubling time and soft agar assays. Activation of MAPK was analyzed using Western blot with phosphospecific monoclonal antibody against dually phosphorylated MAPK. RESULTS: QSG7701 cells transfected with pRcHCNS3-5' showed strong intracellular expression of HCVNS3 protein, and the positive signal was localized in cytoplasm. The expressing strength of HCVNS3 protein in pRcHCNS3-3'-transfected cells was weaker than that in pRcHCNS3-5'-transfected cells. The population doubling time in the transfected cells with pRcHCNS3-5' (12 h) was much shorter than those with pRcHCNS3-3', pRcCMV and normal cells (24, 26, 28 h, respectively) (P<0.01). The transfected cells with pRcHCNS3-5' showed much more anchorage independent colonies than that in those with pRcHCNS3-3' and pRcCMV (P<0.01). The cloning efficiencies of transfected cells with pRcHCNS3-5', pRcHCNS3-3', pRcCMV and controls were 33%, 1.33%, 1.46%, 1.11% respectively. The level of phosphorylated MAPK in the cells with pRcHCNS3-5' was much higher than that in those with pRcHCNS3-3'and pRcCMV and normal cells (P<0.01). CONCLUSION: The results suggest that (1) QSG7701 cells are a better human liver cell line for investigating the pathogenesis of HCV NS3 protein. (2) 5' region of the HCV genome segment encoding HCV NS3 is involved in cell growth and cell phenotype. (3) HCV NS3 N-terminal peptide may up-regulate the activation of MAPK, but not affect the expression of MAPK.

Cell Division↗
PubMed2005

Effect of morphine and naloxone on release of the excitatory amino acids of spinal astrocytes induced by TNF-alpha.

The effect of morphine and naloxone on release of the excitatory amino acids (EAAs) of spinal astrocytes induced by TNF-a was studied. Astrocytes were purified from 2- to 3-day old SD rats and divided into 8 groups: group 1 (without any stimulatants); group 2 (10 ng/ml TNF-alpha); group3 (10 ng/ml TNF-alpha + 0.5 micromol/L morphine); group 4 (10 ng/ml TNF-alpha + 1.0 micromol/L morphine); group 5 (10 ng/ml TNF-alpha + 2. 0 micromol/L morphine); group 6 (10 ng/ml TNF-alpha + 0.5 micromol/L naloxone); group 7 (10 ng/ml TNF-alpha + 1.0 0Lmol/L naloxone); group 8 (10 ng/ml TNF-alpha + 2. 0 micromol/L naloxone). In group 2, 3, 4 and 5, 0, 0.5, 1.0 or 2.0 micromol/L morphine was added to the cells cultured with serum-free Neurobasal/B27 medium containing 10 ng/ml TNF-alpha respectively, while in group 6, 7 and 8, 0.5, 1.0 or 2.0 micromol/L naloxone was added respectively to the cells cultured with serum-free Neurobasal/B27 medium containing 10 ng/ml TNF-alpha. After 30 min incubation, high-pressure liquid chromatography (HPLC) was used to measure the levels of EAAs in all cultured cells. The results showed the level of EAAs in group 2 was significant higher than in group 1 (P < 0.01). As compared with group 2, the levels of EAAs in group 3, 4 and 5 were decreased with the difference being significant between group 5 and group 2 (P < 0.01) or between group 4 and group 2 (P < 0.05). The levels of EAAs in group 6, 7 and group 8 was significantly lower than in group 2 (P < 0.05 or P < 0.01). It was concluded that TNF-alpha could promote the release of glutamate and aspartate from astrocytes, and morphine and naloxone might reduce the release of EAAs in cultured spinal astrocytes induced by TNF-alpha.

Animals↗
PubMed2005

Polyclonal antibody against Manduca sexta chitinase and detection of chitinase expressed in transgenic cotton.

The chitinase gene of Manduca sexta was cloned into the expression vector, pET-28a, and expressed in Escherichia coli BL21 (DE3) host cells. The protein product was expressed in inclusion bodies. After denaturation and renaturation procedures using a Ni2+-NTA affinity chromatography column, soluble chitinase was obtained. The authenticity of the renatured protein was confirmed by Western blotting. Polyclonal antibodies to the purified protein were raised in rabbits. The antibody reacted specifically with the expressed chitinase and was used to quantify its presence in transgenic cotton being developed to resist attack by various insects.

Animals↗
PubMed2005

Efficient enzymatic synthesis of 4-methylumbelliferyl N-acetyllactosaminide and 4-methylumbelliferyl sialyl N-acetyllactosaminides employing beta-D-galactosidase and sialyltransferases.

4-Methylumbelliferyl N-acetyllactosaminide and 4-methylumbelliferyl sialyl N-acetyllactosaminides, which are used for the assay of sialytransferase, neuraminidase and fucosyltransferase, were synthesized, respectively, by the beta-D: -galactosidase from Bacillus circulans and by a recombinant rat alpha2,3-(N)-sialyltransferase or rat liver alpha2,6-(N)-sialyltransferase with CMP-N-acetylneuraminic acid as donor.

Acetylglucosamine↗
PubMed2005

An experimental study of dendritic cells-mediated immunotherapy against intracranial gliomas in rats.

OBJECT: To investigate the effect of dendritic cells(DC) pulsed with apoptotic tumor cells for treatment of intracranial gliomas in rats. METHODS: C6 glioma cells were injected into brain of Wistar rats under stereotactic monitor to establish an animal model of glioma. The precursors of DCs were isolated from bone marrow of rats, stimulated in vitro with recombinent rat granulocyte-macrophage colony-stimulating factor (rrGM-CSF) and interleukin-4 (rrIL-4). These DCs were then pulsed ex vivo with apoptotic C6 glioma cells induced by heating and subsequently injected subcutaneously into rats harboring intracranial C6 glioma. Rats were treated with five weekly subcutaneous injections of either control media, unpulsed DCs, or DCs pulsed with apoptotic tumor cells. The animals were followed for survival, volume of tumor by MRI, CD8 + T cells, cytotoxicity assay in vitro and proliferational function of lymphocytes in peripheral blood were determined by flow cytometry(FCM). The concentration of cytokines interferon-gamma (IFN-gamma) and interleukin-10(IL-10) were monitored through enzyme-linked immunosorbent assay(ELISA) using ELISAkit. RESULTS: Our results indicated that C6 glioma model rats treated with apoptotic tumor cells pulsed DCs prolonged survival, inhibited the tumor growth and increased the level of CD8 + T lymphocytes in peripheral blood comparing with control group. Cytotoxicity assay suggested that vaccination with these apoptotic cells pulsed DCs can induce cytotoxic T lymphocytes response against C6 tumor cells compared with control group. Furthermore, significantly enhanced IFN-gamma and reduced IL-10(even undetectable) were observed in peripheral blood of rats treated with pulsed-DCs. No evident autoimmune response were detected. CONCLUSIONS: Our data demonstrated that systemic vaccination with DCs pulsed with apoptotic cells is a safe and effective immunotherapy for intracranial glioma.

Animals↗
PubMed2005

Overview of approaches for screening for ubiquitin ligase inhibitors.

E3 ubiquitin ligases are a large family of proteins that, together with ubiquitin-activating enzyme E1 and ubiquitin-conjugating enzyme E2, catalyze the ubiquitination of a variety of protein substrates for targeted degradation by means of the 26S proteasome. Because the turnover of many proteins involves targeted ubiquitination and degradation, E3 ubiquitin ligases, therefore, regulate almost every aspect of eukaryotic cellular functions or biological processes. Accumulated evidence in the past few years has suggested that a subset of E3 ubiquitin ligases that regulates the turnover of tumor suppressors and cell cycle regulators could be promising targets for mechanism-driven cancer drug discovery. Thus, it is highly desirable to optimize the methods of high-throughput screening (HTS) for specific inhibitors of these E3 ubiquitin ligases. Here I will give an overview of several approaches used for HTS for ubiquitin ligase inhibitors with a main focus on assay principles, applications, and the pros and cons of each approach. Experimental details for many of these assays can be found in other chapters in this volume.

Drug Evaluation, Preclinical↗
PubMed2005

Characterization of the interactions of the nephrin intracellular domain.

Nephrin is a signalling cell-cell adhesion protein of the Ig superfamily and the first identified component of the slit diaphragm that forms the critical and ultimate part of the glomerular ultrafiltration barrier. The extracellular domains of the nephrin molecules form a network of homophilic and heterophilic interactions building the structural scaffold of the slit diaphragm between the podocyte foot processes. The intracellular domain of nephrin is connected indirectly to the actin cytoskeleton, is tyrosine phosphorylated, and mediates signalling from the slit diaphragm into the podocytes. CD2AP, podocin, Fyn kinase, and phosphoinositide 3-kinase are reported intracellular interacting partners of nephrin, although the biological roles of these interactions are unclarified. To characterize the structural properties and protein-protein interactions of the nephrin intracellular domain, we produced a series of recombinant nephrin proteins. These were able to bind all previously identified ligands, although the interaction with CD2AP appeared to be of extremely low stoichiometry. Fyn phosphorylated nephrin proteins efficiently in vitro. This phosphorylation was required for the binding of phosphoinositide 3-kinase, and significantly enhanced binding of Fyn itself. A protein of 190 kDa was found to associate with the immobilized glutathione S-transferase-nephrin. Peptide mass fingerprinting and amino acid sequencing identified this protein as IQGAP1, an effector protein of small GTPases Rac1 and Cdc42 and a putative regulator of cell-cell adherens junctions. IQGAP1 is expressed in podocytes at significant levels, and could be found at the immediate vicinity of the slit diaphragm. However, further studies are needed to confirm the biological significance of this interaction and its occurrence in vivo.

Amino Acid Sequence↗
PubMed2005

SAK, a new polo-like kinase, is transcriptionally repressed by p53 and induces apoptosis upon RNAi silencing.

Chip profiling of a p53 temperature-sensitive tumor model identified SAK (Snk/Plk-akin kinase), encoding a new member of polo-like kinases (PLKs), as a gene strongly repressed by wild-type p53. Further characterization revealed that SAK expression was downregulated by wild-type p53 in several tumor cell models. Computer search of a 1.7-kb SAK promoter sequence revealed three putative p53 binding sites, but p53 failed to bind to any of these sites, indicating that SAK repression by p53 was not through a direct p53 binding to the promoter. Transcriptional analysis with luciferase reporters driven by SAK promoter deletion fragments identified SP-1 and CREB binding sites, which together conferred a two-fold SAK repression by p53. However, the repression was not reversed by cotransfection of SP-1 or CREB, suggesting a lack of interference between p53 and SP-1 or CREB. Significantly, p53-mediated SAK repression was largely reversed in a dose-dependent manner by Trichostatin A, a potent histone deacetylase (HDAC) inhibitor, suggesting an involvement of HDAC transcription repressors in SAK repression by p53. Biologically, SAK RNA interference (RNAi) silencing induced apoptosis, whereas SAK overexpression attenuated p53-induced apoptosis. Thus, SAK repression by p53 is likely mediated through the recruitment of HDAC repressors, and SAK repression contributes to p53-induced apoptosis.

Amino Acid Sequence↗
PubMed2005

Hard tick calreticulin (CRT) gene coding regions have only one intron with conserved positions and variable sizes.

Calreticulin (CRT) is a unique eukaryotic gene. The CRT gene product, calreticulin, was first identified as a calcium binding protein in 1974, but further investigations have indicated that CRT protein performs many functions in cells, including involvement in evading the host's immune system by parasites. Many studies of CRT have been published since the molecule was first discovered; however, the CRT gene exon-intron structure is only known for a limited number of ectoparasite species. In this study, we compared tick CRT genomic sequences to the corresponding cDNA from 28 species and found that 2 exons and 1 intron are present in the tick CRT gene. The intron position is conserved in 28 hard ticks, but intron size and nucleotide sequences vary. Three tick introns possess duplicated fragments and are twice as long as other introns. All tick CRT introns obey the GT-AG rule in the splice-site junctions and are phase 1 introns. By comparing tick CRT introns to those of fruit fly, mouse, and human, we conclude that tick CRT introns belong to the intron-late type. The number and size of CRT introns have increased through the evolution of eukaryotes.

Animals↗