Nucleotide Sequences Of Introns Research Articles

A polymorphism in intron I of the human angiotensinogen gene (hAGT) affects binding by HNF3 and hAGT expression and increases blood pressure in mice

Angiotensinogen (AGT) is the precursor of one of the most potent vasoconstrictors, peptide angiotensin II. Genome-wide association studies have shown that two A/G polymorphisms (rs2493134 and rs2004776), located at +507 and +1164 in intron I of the human AGT (hAGT) gene, are associated with hypertension. Polymorphisms of the AGT gene result in two main haplotypes. Hap-I contains the variants -217A, -6A, +507G, and +1164A and is pro-hypertensive, whereas Hap-II contains the variants -217G, -6G, +507A, and +1164G and does not affect blood pressure. The nucleotide sequence of intron I of the hAGT gene containing the +1164A variant has a stronger homology with the hepatocyte nuclear factor 3 (HNF3)-binding site than +1164G. Here we found that an oligonucleotide containing +1164A binds HNF3β more strongly than +1164G and that Hap-I-containing reporter gene constructs have increased basal and HNF3- and glucocorticoid-induced promoter activity in transiently transfected liver and kidney cells. Using a knock-in approach at the hypoxanthine-guanine phosphoribosyltransferase locus, we generated a transgenic mouse model containing the human renin (hREN) gene and either Hap-I or Hap-II. We show that transgenic animals containing Hap-I have increased blood pressure compared with those containing Hap-II. Moreover, the transcription factors glucocorticoid receptor, CCAAT enhancer-binding protein β, and HNF3β bound more strongly to chromatin obtained from the liver of transgenic animals containing Hap-I than to liver chromatin from Hap-II-containing animals. These findings suggest that, unlike Hap-II variants, Hap-I variants of the hAGT gene have increased transcription rates, resulting in elevated blood pressure.

Abstract 129: The Role of Intron-2 Conversion Polymorphism in the Regulation of Human Aldosterone Synthase Gene Expression

The hCYP11B2 gene encodes aldosterone synthase, the rate-limiting enzyme in the biosynthesis of aldosterone. Inappropriate excess levels of aldosterone induces positive sodium balance and predisposes to hypertension and other cardiovascular problems. hCYP11B2 has a T/C polymorphism located at -344 in its promoter region. This variant is in close linkage disequilibrium with a complex hCYP11B2 Intron 2 conversion polymorphism (IC), which replaces a segment of DNA within intron 2 with the corresponding region of hCYP11B1. Epidemiological studies have suggested that -344 T/C and the IC polymorphism associating with hypertension. The IC polymorphism always occur when the promoter contains -344T variant. In the present study we have for the first time sequenced the full length hCYP11B2 intron 2 from randomly selected hypertensive samples from the Caucasian cohort and identified the segment of hCYP11B2 replaced by that of hCYP11B1 Intron2. It is interesting to note that in these genomic DNA samples there is no change in the hCYP11B1 intron2 sequence. In silico transcription factor binding site predictions indicate that there are several transcription factors which can bind more strongly to the hCYP11B2 IC region as compared to wild type intron2 (wt). We have cloned the IC polymorphism and the wt intron nucleotide sequences in front of the 1kb hCYP11B2 promoter containing -344T. These reporter constructs showed differential transcriptional activation. Basal promoter activity of IC intron was increased by 1.94 fold (p<0.05) compared to that of wt intron2. Further co-transfection studies of these reporter constructs along with transcription factors HNF3B and NFkB showed significantly increased relative luciferase activity of 2.9 and 3.26 fold (p<0.05) in IC construct as compared to wt intron respectively. These results strongly suggest that IC in hCYP11B2 has strong regulatory elements as compared to the wt intron leading to enhanced transcriptional activity and thus increased hCYP11B2 gene expression. This would increase tissue or plasma aldosterone levels in human subjects containing IC polymorphism. The long term consequence of altered regulation of aldosterone production can lead to an increase in blood pressure and cardiovascular complications.

The OitaAG and OitaSTK genes of the orchid Orchis italica: a comparative analysis with other C- and D-class MADS-box genes

According to the ABCDE model of flower development, the C- and D- class MADS box genes are involved in the formation of male and female reproductive organs (fused to form the column in orchids) and in ovule maturation (triggered by fertilization in orchids). In the present study, we report the isolation of the Orchis italica genes OitaAG and OitaSTK, homologs of the C-class AGAMOUS and the D-class SEEDSTICK genes of Arabidopsis, respectively. Analysis of their expression profiles reveals high levels of mRNA in columns and ovaries, particularly after pollination. However, weak expression is also detectable in the inner tepals (OitaAG) and the lip and root (OitaSTK). This expression profile is only partially overlapping with those reported in other orchid species and may be the consequence of a different evolutionary history of these functional gene classes in orchids. The genomic characterization of the OitaAG and OitaSTK genes shows that a high number of traces of mobile elements are present in introns and could have contributed to the size expansion of some of them (e.g., intron 2 and 3 of OitaAG and intron 3, 4 and 5 of OitaSTK). Nucleotide sequences of intron 1 of the OitaSTK gene and other STK-like genes do not share regulatory motifs, whereas sequence comparison of intron 2 of the OitaAG gene with that of intron 2 of other AG-like genes reveals, for the first time in an orchid species, the presence of conserved cis-regulatory boxes and binding sites for transcription factors that positively (e.g., LEAFY and WUSCHEL) or negatively (e.g., BELLRINGER) regulate the expression of the AG homologs in dicots and monocots.

Dimorphic Goat Amelogenin Alleles on Sex Chromosomes for Gender Determination of Preimplantation Embryos

 Abstract—Amelogenin (AMEL) is a conserved gene located on the sex chromosomes of mammals. It is involved in the formation of enamel, which is the hard, white material that forms the protective outer layer of each tooth. In this study, we first cloned the coding sequences of the goat AMELX and AMELY transcripts from female and male lamb enamel tissues during tooth development. All 207 amino acids of the putative AMEL proteins from the cDNA coding regions of both sex chromosomes were the same, but the AMEL sequences of the 3’-untranslated regions (UTR) were different. The results showed that the nucleotide sequences of intron 5 of the goat AMELX and AMELY genes contained multiple deletions/insertions and had only 48.5% identity. Based on the dimorphic AMEL intron sequences, a set of sex-specific primers was successfully applied to goat gender determination. A high sensitivity for sex determination was reached with a minimal amount of template, such as a trace amount of genomic DNA from a single blastomere isolated from embryos at the blastula stage among different strains of goats.

The genomic structure and the expression profile of the Xenopus laevis transthyretin gene

Transthyretin (TTR) is a major thyroid hormone-binding protein in the amphibian tadpole whose plasma mRNA and protein levels are altered during metamorphosis. While the temporal and spatial expression patterns and genomic structure of the TTR gene are well studied in higher vertebrates, detailed expression pattern in the extrahepatic tissues, the transcriptional regulation, and the genomic structure have not yet been identified in amphibians. In this study, we attempted to elucidate these mechanisms. Here, we determined the genomic structure of the Xenopus laevis TTR gene including 5′-flanking regions, and examined TTR expression patterns in several tissues. The TTR gene of X. laevis is composed of 4 exons and 3 introns, and the nucleotide sequence of intron 1 is not similar to that previously reported. This suggests that the TTR gene of X. laevis was duplicated and the gene cloned in this study was the other copy of previously reported gene. We also found that TTR was primarily transcribed in the liver of both tadpoles and adults. In the adult liver, TTR transcripts were more abundant in males than females. In higher vertebrates, the expression of TTR is controlled by several transcription factors including forkhead box A2 (FoxA2). However, in the X. laevis liver, FoxA2 expression patterns were not similar to TTR. We also found that exogenous FoxA2 increased the X. laevis TTR promoter-driven luciferase activity. These results suggest that, in amphibian, the expression of TTR is regulated partially by FoxA2, and that another system may exist to control TTR expression.

Genetic and Evolutionary Correlates of Fine-Scale Recombination Rate Variation in Drosophila persimilis

Recombination is fundamental to meiosis in many species and generates variation on which natural selection can act, yet fine-scale linkage maps are cumbersome to construct. We generated a fine-scale map of recombination rates across two major chromosomes in Drosophila persimilis using 181 SNP markers spanning two of five major chromosome arms. Using this map, we report significant fine-scale heterogeneity of local recombination rates. However, we also observed "recombinational neighborhoods," where adjacent intervals had similar recombination rates after excluding regions near the centromere and telomere. We further found significant positive associations of fine-scale recombination rate with repetitive element abundance and a 13-bp sequence motif known to associate with human recombination rates. We noted strong crossover interference extending 5-7Mb from the initial crossover event. Further, we observed that fine-scale recombination rates in D.persimilis are strongly correlated with those obtained from a comparable study of its sister species, D.pseudoobscura. We documented a significant relationship between recombination rates and intron nucleotide sequence diversity within species, but no relationship between recombination rate and intron divergence between species. These results are consistent with selection models (hitchhiking and background selection) rather than mutagenic recombination models for explaining the relationship of recombination with nucleotide diversity within species. Finally, we found significant correlations between recombination rate and GC content, supporting both GC-biased gene conversion (BGC) models and selection-driven codon bias models. Overall, this genome-enabled map of fine-scale recombination rates allowed us to confirm findings of broader-scale studies and identify multiple novel features that merit further investigation.

Self-incompatibility alleles in Polish wild pear (Pyrus pyraster (L.) Burgsd.): a preliminary analysis

Wild pear (Pyrus pyraster, syn. P. communis var. pyraster) is thought to be one of the species that gave rise to all other members of the genus Pyrus, although intraspecific hybridizations with cultivated varieties could cause the disappearance of original species characteristics. S-RNase alleles from 7 different wild pear individuals, collected from various regions of Poland, were cloned on the basis of the PCR method and nucleotide sequence analyses. The hypervariable (HV) region is responsible for allele-specific S-RNase activity in the self-incompatibility mechanism. The high level of polymorphism of its sequences may constitute a source of valuable phylogenetic information. From all individuals, 14 sequences were obtained successfully, and 9 of them were novel alleles. Phylogenetic analysis of these alleles was based on the amino acid sequence interpretation of coding regions and intron nucleotide sequences. The research conducted on a limited pool of available P. pyraster alleles gives only an initial insight into possible S-RNase allele polymorphisms in wild populations. At this stage, the results do not confirm a strong influence of cultivated pear species on the wild pear.

Molecular diagnosis of Candida albicans using real-time polymerase chain reaction of a CaYST1 gene

Candida albicans is an opportunistic pathogen that causes infections in immuno-compromised individuals. Virulence of this organism is a function of a multiplicity of factors working jointly to overwhelm the host defenses. From a previous study, the in vitro adherence capabilities of seven isolates (collected from patients suffering vaginitis) to vaginal epithelial cells were tested. Isolate No. 2 recorded the highest adherence ability. In this part of work, Real-time PCR assay was applied for the identification of isolate No. 2. This isolate could be discriminated by species-specific primers, deduced from the intron nucleotide sequence of the C. albicans CaYST1 gene. To confirm that the isolated strain is a fungal strain, the universal fungal primers (ITS5 and ITS4) were used to amplify the complete internal transcribed spacer (ITS) region including the 5.8S ribosomal gene that is present in all fungi. The ITS region was successfully amplified from the tested yeast, provided a single PCR product of approximately 520 bp. In another run, a single pair of specific primers [Intron Nucleotide Sequence (INT1 and INT2)] was then used to amplify the intron nucleotide sequence of the CaYST1 gene, which present only in C. albicans. The generated amplified product gave the expected single band of 310 bp. The melting points of all PCR products were routinely determined. The results showed that the melting temperatures for the tested isolate and the reference strain of C. albicans (ATCC 10231) using ITS5 and ITS4 primers were 80.09°C and 83.99°C, respectively, while they were 80.78°C and 80.10°C using INT1 and INT2 when assayed individually. Based on their very close melting profiles, the tested isolate proved to be identical to C. albicans reference strain. These results supported the idea of using genes containing intron sequences to design species-specific primers for the identification of fungal strains by real time PCR.

Pivotal Advance: Eosinophilia in the MES rat strain is caused by a loss–of–function mutation in the gene for cytochrome b(–245), alpha polypeptide (Cyba)

MES is a rat strain that spontaneously develops severe blood eosinophilia as a hereditary trait. Herein, we report that eosinophilia in MES rats is caused by a loss-of-function mutation in the gene for cytochrome b(-245), alpha polypeptide (Cyba; also known as p22(phox)), which is an essential component of the superoxide-generating NADPH oxidase complex. The MES rat has a deletion of four nucleotides, including the 5' splice donor GpT of intron 4 of the Cyba gene. As a consequence of the deletion, a 51-nucleotide sequence of intron 4 is incorporated into the Cyba transcripts. Leukocytes from the MES strain lack both CYBA protein and NADPH oxidase activity. Nevertheless, unlike patients with chronic granulomatous disease, who suffer from infections with pathogens due to similar genetic defects in NADPH oxidase, MES rats retain normal innate immune defense against Staphylococcus aureus infection. This is due to large quantities of peritoneal eosinophils in MES rats, which phagocytose and kill the bacteria. MES rat has a balance defect due to impaired formation of otoconia in the utricles and saccules. Eosinophilia of the MES rat was normalized by introduction of a normal Cyba transgene. The mechanisms by which impairment of NADPH oxidase leads to eosinophilia in the MES rat are elusive. However, our study highlights the essential role of NADPH oxidase in homeostatic regulation of innate immunity beyond conventional microbicidial functions.

Partial genomic organization of ribosomal protein S7 gene from malaria vector Anopheles stephensi

AbstractIn this study, we describe the partial genomic organization of ribosomal protein S7 gene isolated from the mosquito Anopheles stephensi. Initially a 558 bp partial cDNA sequence was amplified as precursor mRNA sequence containing 223 bp long intron. 5′ and 3′ end sequences were recovered using end specific rapid amplification of cDNA ends (RACE) polymerase chain reaction. The full‐length cDNA sequence was 914 nucleotide long with an open reading frame capable of encoding 192 amino acid long protein with calculated molecular mass of 22 174 Da and a pI point of 9.94. Protein homology search revealed > 75% identity to other insect's S7 ribosomal proteins. Analysis of sequence alignment revealed several highly conserved domains, one of which is related to nuclear localization signal (NLS) region of human rpS7. Interestingly, intron nucleotide sequence comparison with A. gambiae showed a lesser degree of conservation as compared to coding and untranslated regions. Like this, early studies on the genomic organization and cDNA/ Expressed sequence tag analysis (EST) could help in genome annotation of A. stephensi, and would be likely to be sequenced in the future.

The identity of the Javan Krait, Bungarus javanicus Kopstein, 1932 (Squamata: Elapidae): evidence from mitochondrial and nuclear DNA sequence analyses and morphology

The Javan Krait (Bungarus javanicus Kopstein, 1932) was described on the basis of a single specimen that had been discovered subsequent to its delivery of lethal bites to two sleeping people in a rice field hut. Until 1936, only two additional specimens were found in the vicinity of the type locality near Cirebon on the north coast of West Java province, Indonesia. The taxonomic status of B. javanicus has remained doubtful due to its great similarity to the common and widely distributed Malayan Krait (Bungarus candidus), from which it was distinguished only by its black (vs. black-andwhite banded) colouration. We rediscovered B. javanicus near its type locality in 1993 and obtained substantial series of black kraits in West and Central Java provinces in 1996 and 1998. We provide a detailed redescription of the type specimen and the two other specimens of B. javanicus available to Kopstein. We then use nucleotide sequences of the mitochondrial cytochrome b gene to estimate relationships among 27 black and black-and-white banded kraits from Java and Bali. In addition, we use exon-primed intron-crossing primers to analyze a sequence segment of the alpha-bungarotoxin (A31) gene from ten black and black-and-white banded kraits from these islands. Four mitochondrial haplotypes were identified which exhibited minimal sequence divergence and no correlation to colouration. In particular, both external phenotypes were found in the same genealogical lineage near Indramayu, where black kraits and black-and-white banded B. candidus occur in syntopy. Neither the nucleotide sequence of intron 2 nor partial exon 2 and 3 sequences of the alphabungarotoxin (A31) gene exhibited variation within the sample from Java and Bali. Intron 2 sequence divergence between the Javan kraits and the closely related Bungarus multicinctus is 1.1%. Morphological examination of specimens of B. javanicus and B. candidus from Java revealed no differences beyond colouration. The combined evidence identifies the locally strong populations of black kraits in Java as conspecific with local B. candidus. Their regional dichromatism includes two fundamentally different patterns for predator avoidance, and is interpreted as the result of increased genetic fixation of mutations in one or several instable genes (which can cause similar pattern abnormalities in various species of Bungarus), in the course of the colonization of the alluvial plains of northern Java. These plains are of very recent origin and likely offered selective pressures different from those in older parts of the island, rendering both black and black-and-white banded phenotypes successful in predator avoidance.

Further evidence for recombination between mouse hemoglobin beta b1 and b2 genes based on the nucleotide sequences of intron, UTR, and intergenic spacer regions

Nucleotide sequences of the intron regions and UTRs (Untranslated regions) of the hemoglobin beta adult genes, b1 and b2, and of the intergenic spacer region were determined for mouse strains representing the d, p, and w1 hemoglobin haplotypes defined by protein electrophoretic analyses. The hypothesis of recombination of the b1 and b2 genes between the d and w1 haplotypes previously reported in the cDNA nucleotide sequences was confirmed by neighbor-joining analyses of the intron regions and UTRs within the b1 and b2 genes, suggesting that all of the structures of hemoglobin beta adult genes support the hypothesis that the p haplotype was established by hybridization between d and w1 haplotype mice. The resultant recombinant of the p haplotype was found to have a d-like b1 gene and a w1-like b2 gene. In addition to the possible recombination, a break point was suggested around 2-3 kb downstream of the b1 gene within the intergenic spacer region, despite the absence of clear properties that could stimulate the recombination machinery. Some large insertions or deletions (indels) specific to the p or d haplotypes were located within the intergenic spacer region, in which the 1010-bp indel specific to the p haplotype was shared by all examined strains representing the p haplotype.

Screening for mutations in the lipopolysaccharide‐induced tumor necrosis factor‐alpha factor (litaf) gene in italian patients with charcot‐marie‐tooth disease.

Mutations in LITAF (lipopolysaccharide‐induced tumor necrosis factor‐alpha factor), also referred to as SIMPLE, are associated with one of the dominantly inherited demyelinating forms of Charcot‐Marie‐Tooth disease (CMT1C). LITAF is a widely expressed gene, which maps on chromosome 16p13.1‐p12.3 and encodes a 161‐amino acid protein that may play a role in the degradation of proteins critical to peripheral nerve function. A cohort of 46 unrelated Italian patients affected with demyelinating peripheral neuropathy with dominant inheritance was screened for mutations in the LITAF gene. The three coding exons (2, 3 and 4) and flanking intron nucleotide sequence was examined by single strand conformation polymorphism (SSCP) and direct sequencing. All patients were negative for the 17p11.2 duplication and for mutations in the MPZ, PMP22 and EGR2 genes. SSCP analysis showed several electrophoretic variants in all exons. Direct sequencing demonstrated the presence of few single nucleotide substitutions. All of them were demonstrated to be common polymorphisms: one of them was non‐synonymous, two were synonymous and two were intronic. Based on the present analysis, LITAF mutations are not a frequent cause of autosomal dominant demyelinating neuropathies in our population.

IGS sequence variation, group-I introns and the complete nuclear ribosomal DNA of the entomopathogenic fungus Metarhizium: excellent tools for isolate detection and phylogenetic analysis

The complete nuclear rDNA gene complex of Metarhizium anisopliae var. anisopliae isolate ME1 is 8118 bp long and contains the 18S, 5.8S, and 28S rRNA genes as well as the ITS and IGS regions. Variation in the ITS of isolates of M. anisopliae var. anisopliae and one each of Metarhizium anisopliae var. acridum, Metarhizium flavoviride var. flavoviride, and Metarhizium flavoviride var. minus, clustered 39 out of 40 of M. anisopliae var. anisopliae isolates in one clade. Nucleotide sequence variation in the IGS among 21 of M. anisopliae var. anisopliae isolates showing IGS length variation sorted them into three strongly supported clades, which were weakly correlated with insect hosts and were not correlated with geographic location. Two group-I introns, Ma-int4 and Ma-int5, were discovered in the 18S and the 3 ′ end of the 28S, in M. anisopliae var. anisopliae isolates ITALY-12 and IMBST 9601. The insertion sites and sub-group of these introns correlated with their closest relatives, as judged by phylogenetic analysis of intron nucleotide sequence.

Molecular features of a defined genetic marker for the determination of the Porphyra tenera lineage

Nucleotide sequences of the nuclear SSU rDNA and ITS1 are presented as a defined genetic marker for Porphyra tenera as a species. Exon nucleotide sequences were identical within all the P. tenera specimens. Intron nucleotide sequences varied between populations. The introns and ITS1 variations are presented as defined genetic markers to establish the Porphyra tenera strains. Wild-collected thalli identified by morphological systematics, from five populations of Porphyra tenera throughout Japan, were discriminated by comparing sequences of the various regions utilizing the results of this and previous studies.

Isolates of Microbotryum violaceum from North American host species are phylogenetically distinct from their European host-derived counterparts

Microbotryum violaceum is a basidiomycete that infects the anthers of its Caryophyllaceae host species. Individual fungal isolates are host limited, though they are not morphologically distinct. This study used variable regions of the highly conserved gamma-tubulin, beta-tubulin, and ribosomal RNA-encoding genes to determine the relationships among M. violaceum fungal isolates from different host species and different geographical locations. Phylogenetic trees from intron nucleotide sequences in two protein-coding genes were compared to trees produced from internal transcribed spacers (ITS) of rDNA. Phylogenetic analyses suggested that there are two clades, one from North America and one from Europe. Isolates from both clades grouped according to host species, although in some analyses isolates from closely related host species were placed together. These results are consistent with the view that M. violaceum has experienced cospeciation with its hosts.

A weak blood group A phenotype caused by a new mutation at the ABO locus.

A number of alleles have been described for ABO encoding for common and rare ABO blood group phenotypes. Critical mutations in the coding sequence of ABO that may confer the different specificity and activity of the glycosyltransferases encoded by this gene locus have been identified. Three unrelated patients from Germany, Turkey, and Bosnia who were diagnosed as having variant A subgroups were subjected to extended ABO typing. Serologic investigations were performed with standard methods. The genetic basis of the ABO phenotypes was determined by haplotype-specific sequence analysis of the last two exons (exons 6 and 7) of ABO and the intervening intron. The RBCs of all three patients showed serologic A characteristics being similar to subgroup A(x). The serum of all three patients contained weakly reactive anti-A. In all three patients, sequence analysis indicated an A allele with a nucleotide sequence identical to ABO(*)A101 except for a single-base substitution in exon 7 at position 502, where C was replaced by G. This point mutation resulted in an amino acid exchange from arginine to glycine at position 168. The nucleotide sequence of intron 6 of the A allele was found to be identical to the ABO(*)A101 sequence in each patient. This study suggests that a variant A phenotype can arise from the new R168G polymorphism, reflecting the importance of this region for the ABO transferase efficiency.

Isolation and sequence analysis of the rat dihydrolipoamide succinyltransferase gene.

The dihydrolipoamide succinyltransferase (DLST) gene of the alpha-ketoglutarate dehydrogenase complex (alpha-KGDC) was isolated from a rat genomic DNA library and sequenced. This gene was composed of 15 exons and 14 introns like the human DLST gene. Sequence analysis of the promoter-regulatory region of the rat DLST gene-(Dlst) showed the possible presence of a CAAT box-sequence and of the sequences for an AP-2 site and three Sp1 sites, but no TATA box-sequence was evidenced. The nucleotide sequences of introns 1 and 4 of the rat Dlst were significantly homologous to those of introns 1 and 4 of the human DLST gene. The sequence analysis of the rat Dlst suggested that the exon coding for the E3- and/or E1-binding domain may have been lost from the gene during evolution in eukaryotic DLST, possibly after mitochondrial symbiosis because prokaryotic DLST possesses the E3- and/or E1-binding domain.

The long form of CDK2 arises via alternative splicing and forms an active protein kinase with cyclins A and E.

We have reinvestigated the long form of cyclin-dependent kinase (CDK)2 that is expressed in many rodent cells. We show that the mRNA encoding CDK2L arises by alternative splicing and that the encoded protein can bind to, and be activated by, cyclins A and E. The complex of CDK2L with cyclin A has about half the specific activity of the equivalent CDK2-cyclin A complex. Also, CDK2L--cyclin A is inhibited to the same extent and by the same concentrations of p21(CIP1) as CDK2--cyclin A. The nucleotide sequences of intron V in the human and murine CDK2 genes, where the sequences encoding the 48-residue insert in CDK2L are located, show very high conservation in the position of the alternatively spliced exon and its surroundings. Despite this, we were not able to detect significant expression of CDK2L in human cell lines, although a low level is expressed in COS-1 cells from monkeys.

ExInt: an Exon/Intron database.

The Exon/Intron (ExInt) database incorporates information on the exon/intron structure of eukaryotic genes. Features in the database include: intron nucleotide sequence, amino acid sequence of the corresponding protein, position of the introns at the amino acid level and intron phase. From ExInt, we have also generated four additional databases each with ExInt entries containing predicted introns, introns experimentally defined, organelle introns or nuclear introns. ExInt is accessible through a retrieval system with pointers to GenBank. The database can be searched by keywords, locus name, NID, accession number or length of the protein. ExInt is freely accessible at http://intron.bic.nus.edu.sg/exint/exint.html