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Covariate linkage analysis of GAW14 simulated data incorporating subclinical phenotype, sex, population, parent-of-origin, and interaction.

BACKGROUND: We evaluate a method for the incorporation of covariates into linkage analysis using the Genetic Analysis Workshop 14 simulated data. Focusing on a randomly chosen replicate (42) we investigated the effect of the 12 subclinical phenotypes, sex, population, and parent-of-origin on the linkage signal from a model-free linkage analysis of Kofendrerd Personality Disorder. RESULTS: We detected a linkage peak on chromosome 1, at about 175 cM, which varied depending upon individuals' status for subclinical phenotype b. A linkage peak on chromosome 3 (310 cM) was found not to depend upon subclinical phenotype status. Further peaks were found on chromosomes 5 (12 cM), 9 (4 cM), and 10 (95 cM), depending on the status of subclinical phenotypes a, k, and c/d/g, respectively. CONCLUSION: Retrospective comparison of our results with the simulation model showed correct identification of disease loci D1-5 on chromosomes 1, 3, 5, 9 and 10, respectively.

Chromosome Mapping↗

Identification and characterization of nine novel human small GTPases showing variable expressions in liver cancer tissues.

Digestion and detoxification are the two most important functions of the liver, and liver cells always keep a high metabolism level and active vesicular traffic. The malfunction of the vesicular traffic system might be a cause of the abnormal biological behavior of cancerous liver cells. The Ras superfamily is known to regulate various steps of vesicular traffic in eukaryotic cells. It would be significant to determine the change of vesicular transport molecules such as the members of Ras superfamily in carcinogenesis of liver cells. In the present study, we have cloned nine novel genes encoding human small GTPases: RAB1B, RAB4B, RAB10, RAB22A, RAB24, RAB25 ARL5, SARA1, and SARA2, among which the former six belong to the RAB family and the latter three belong to the ARF/SAR1 family. The identification of these new genes has greatly enlarged the pool of the Ras superfamily. It is interesting to find that they are upregulated in most of the 11 hepatocellular carcinoma and 1 cholangiohepatoma cases. Furthermore, the expression in 16 normal human adult tissues, the chromosome loci, and the gene structures of the nine genes are also described. The above findings could be valuable for understanding the vesicular transport system and elucidating the molecular basis of liver cancer carcinogenesis.

Amino Acid Sequence↗

Beyond active learning: a case study of teaching practices in an occupation-centered curriculum.

Although occupation-centered curricula are highly promoted, the teaching processes that convey such designs remain unclear. This case study elucidated occupation-centered teaching practices. Interview and observational data were collected over 8 weeks, and analysis involved coding transcriptions, data matrices, concept maps, journaling, and writing. Participants augmented active learning strategies with strategies that linked course topics to the subject of occupation. The use of linking strategies suggested that: (a) course content was treated as two-tiered; (b) neither content nor instructional processes were inherently occupation-centered; and (c) subject-centered education strengthens social learning theories. Although curricula may appear occupation-centered based on a curriculum description and course content, ultimately "linking opportunities" in the classroom constitute an essential feature that demarcates a program as occupation-centered.

Curriculum↗

Identification and characterization of ARHGAP24 and ARHGAP25 genes in silico.

RhoGAP family proteins, encoded by ARHGAP family genes, are negative regulators of Rho family GTPases, which are implicated in actin remodeling, cell polarity control, and cell migration. Based on the homology with ARHGAP22, we identified and characterized two novel ARHGAP family genes, ARHGAP24 and ARHGAP25. FLJ33877 cDNA (AK091196.1) and aberrant DKFZp564- B1162 cDNA (NM_031305.1) were derived from human ARHGAP24 gene. Two isoforms of KIAA0053 type (D29642.1) and BM927439 type were derived from human ARHGAP25 gene due to alternative splicing (alternative promoter). Mouse 0610025G21 (NM_029270.1) and A130039I20 (AK037710.1) were representative cDNAs derived from mouse Arhgap24 and Arhgap25 genes, respectively. Exon-intron structure of ARHGAP25 gene at human chromosome 2p13 was slightly divergent from that of ARHGAP22 and ARHGAP24 genes. MGC35285, MAPK8 and C10orf64 genes linked to ARHGAP22 gene were paralogs of PTPN13, MAPK10 and WDFY3 genes linked to ARHGAP24 gene, respectively. MGC35285-ARHGAP22-MAPK8-C10orf64 locus at human chromosome 10q11 and the WDFY3-ARHGAP24-MAPK10-PTPN13 locus at human chromosome 4q21 were paralogous regions (paralogons) within the human genome. Human ARHGAP24 showed 91.8% and 48.6% total-amino-acid identity with mouse Arhgap24 and human ARHGAP22, respectively. Human ARHGAP25 showed 86.1% and 40.8% total-amino-acid identity with mouse Arhgap25 and human ARHGAP22, respectively. ARHGAP22, ARHGAP24 and ARHGAP25 were found to constitute the RhoGAP subfamily featured by Pleckstrin homology (PH) domain and C-terminal Coiled-coil domain. This is the first report on identification and characterization of the ARHGAP24 and ARHGAP25 genes.

Alternative Splicing↗

[Analysis, identification and correction of some errors of model refseqs appeared in NCBI Human Gene Database by in silico cloning and experimental verification of novel human genes].

We found that human genome coding regions annotated by computers have different kinds of many errors in public domain through homologous BLAST of our cloned genes in non-redundant (nr) database, including insertions, deletions or mutations of one base pair or a segment in sequences at the cDNA level, or different permutation and combination of these errors. Basically, we use the three means for validating and identifying some errors of the model genes appeared in NCBI GENOME ANNOTATION PROJECT REFSEQS: (I) Evaluating the support degree of human EST clustering and draft human genome BLAST. (2) Preparation of chromosomal mapping of our verified genes and analysis of genomic organization of the genes. All of the exon/intron boundaries should be consistent with the GT/AG rule, and consensuses surrounding the splice boundaries should be found as well. (3) Experimental verification by RT-PCR of the in silico cloning genes and further by cDNA sequencing. And then we use the three means as reference: (1) Web searching or in silico cloning of the genes of different species, especially mouse and rat homologous genes, and thus judging the gene existence by ontology. (2) By using the released genes in public domain as standard, which should be highly homologous to our verified genes, especially the released human genes appeared in NCBI GENOME ANNOTATION PROJECT REFSEQS, we try to clone each a highly homologous complete gene similar to the released genes in public domain according to the strategy we developed in this paper. If we can not get it, our verified gene may be correct and the released gene in public domain may be wrong. (3) To find more evidence, we verified our cloned genes by RT-PCR or hybrid technique. Here we list some errors we found from NCBI GENOME ANNOTATION PROJECT REFSEQs: (1) Insert a base in the ORF by mistake which causes the frame shift of the coding amino acid. In detail, abase in the ORF of a gene is a redundant insertion, which causes a reading frame shift in the translation of an alternative protein, such as LOC124919 is wrong form of C17 orf32 (with mouse and rat orthologs determined by us). (2) Put together by mistake (with force). This is a wrong assembly of non-relating cDNA segment, such as LOC147007 is wrong form of C17orf32. (3) Mistakenly insert a base or one section of cDNA in the ORF which causes it ending beforehand, only coding cDNA sequence of N-terminal amino acids, incomplete. For example, LOC123722 is wrong form of SPRYD1, and even the human hypothetical gene LOC126250 or PDCD5 is wrong form of our PDCD5 (TFAR19). (4) Incomplete, only coding cDNA sequence of C-terminal amino acids. For example, human LOC149076 and mouse LOC230761 are wrong form of our verified human ZNF362 and mouse Zfp362, respectively. (5) Incomplete, only coding one section of coding protein cDNA sequence of correct gene ORF, lacking N-terminal and C-terminal amino acids sequence, and at the same time, mistakenly anticipates the first non-initiation codon amino acid of the incomplete protein amino acid as the initiation codon, e.g. anticipating L as M. For example, LOC200084 is wrong form of ZNF362. (6) Mistakenly insert a base or one section of cDNA in the ORF, wrongly causing unwanted termination codon before the insertion, so the coding protein lacks the first part of the amino acids. For example, the GenBank Acc. No. AL096883 ( LOCUS No. HS323M22B) is wrong form of an experimentally verified human NM_012263 with mouse ortholog of BC010510 determined. (7) It may regard the polluted genomic sequence as complete gene cDNA sequence and anticipate the so-called single exon gene, even the real one, only a small ORF in the very long single exon mRNA, while there really exists termination code in the same phase of the upper part of the ORF initiation code, no other characters accord with the gene's condition. For example, LOC91126 is wrong form of ZNF362. (8) The anticipated genes only have ORF which has no EST proofs on both terminal sides. Depending on this ORF, a complete gene cDNA with double support of EST and human genome (there are termination codes at the same phase of the upper part of ORF) which indicates the anticipated ORF reference sequence may be incorrect. For example, LOC164395 may be wrong form of novel human gene bankit4590055. (9) A similar but smaller protein-coding gene is anticipated in the range of the human genome sequence that has the support of EST experimental proof, so other new anticipated gene may be incorrect. For example, LOC167563 may be wrong form of CMYA5. However,these errors can be corrected or avoided by using our strategy. Here we give one example in detail: Comparision of the sequence SPRYD1 with human hypothetical gene LOC123722. The TAA bases in the position of 478-480 in LOC123722 cDNA is redundant, which causes a reading frame shift in the translation of an alternative protein. The redundancy of GTAAA of LOC123722 is not supported by our experimental clone,and is almost fully rejected by human EST alignment, and is shown as the next intron sequence by genomic GT/AG organization analysis. The verification of cDNA or genomic DNA sequence of SPRYD1 implies that LOC123722 has a wrong stop codon within its ORF because of the prediction program, thus being not complete cds. To sum up, by combining bioinformatics analyses with experimental verification, we have found that there are many errors of at least nine kinds appeared in NCBI GENOME ANNOTATION PROJECT REFSEQs through BLAST of our cloned genes in non-redundant database, and our strategy is helpful in correcting them, such as LOC14907, LOC200084 and LOC91126 (all of them should be ZNF362, but are three different kinds of wrong forms of ZNF362), three model reference sequences predicted from NCBI contig NT_004511 by automated computational analysis using gene prediction method, or such as LOC124919 and LOC147007 (both should be C17orf32, but are two different kinds of wrong forms of C17orf32), two model reference sequences predicted from NCBI contig NT_010808 by automated computational analysis using gene prediction method. Therefore, the correct identification and annotation of novel human genes may be still a heavy task, which can be finished within a long period of time. So human genome coding regions annotated by computer should be used with caution. The articles published in the past did not clearly point out the existence of mistakes in the NCBI human gene mode reference sequence. At the Seventh International Human Genome Conference held in April 2002, we first published the researching result on this aspect in the communication form of Posterly insert a base or one section of cDNA in the ORF, wrongly causing unwanted termination codon before the insertion, so the coding protein lacks the first part of the amino acids. For example, the GenBank Acc. No. AL096883 ( LOCUS No. HS323M22B) is wrong form of an experimentally verified human NM_012263 with mouse ortholog of BC010510 determined. (7) It may regard the polluted genomic sequence as complete gene cDNA sequence and anticipate the so-called single exon gene, even the real one, only a small ORF in the very long single exon mRNA, while there really exists termination code in the same phase of the upper part of the ORF initiation code, no other characters accord with the gene's condition. For example, LOC91126 is wrong form of ZNF362. (8) The anticipated genes only have ORF which has no EST proofs on both terminal sides. Depending on this ORF, a complete gene cDNA with double support of EST and human genome (there are termination codes at the same phase of the upper part of ORF) which indicates the anticipated ORF reference sequence may be incorrect. For example, LOC164395 may be wrong form of novel human gene bankit4590055. (9) A similar but smaller protein-coding gene is anticipated in the range of the human genome sequence that has the support of EST experimental proof, so other new anticipated gene may be incorrect. For example, LOC167563 may be wrong form of CMYA5. However, these errors can be corrected or avoided by using our strategy. Here we give one example in detail: Comparision of the sequence SPRYD1 with human hypothetical gene LOC123722. The TAA bases in the position of 478-480 in LOC123722 cDNA is redundant, which causes a reading frame shift in the translation of an alternative protein. The redundancy of GTAAA of LOC123722 is not supported by our experimental clone, and is almost fully rejected by human EST alignment, and is shown as the next intron sequence by genomic GT/AG organization analysis. The verification of cDNA or genomic DNA sequence of SPRYD1 implies that LOC123722 has a wrong stop codon within its ORF because of the prediction program, thus being not complete cds. To sum up, by combining bioinformatics analyses with experimental verification, we have found that there are many errors of at least nine kinds appeared in NCBI GENOME ANNOTATION PROJECT REFSEQs through BLAST of our cloned genes in non-redundant database, and our strategy is helpful in correcting them, such as LOC14907, LOC200084 and LOC91126 (all of them should be ZNF362, but are three different kinds of wrong forms of ZNF362), three model reference sequences predicted from NCBI contig NT_004511 by automated computational analysis using gene prediction method, or such as LOC124919 and LOC147007 (both should be C17orf32, but are two different kinds of wrong forms of C17orf32), two model reference sequences predicted from NCBI contig NT_010808 by automated computational analysis using gene prediction method. Therefore, the correct identification and annotation of novel human genes may be still a heavy task, which can be finished within a long period of time. So human genome coding regions annotated by computer should be used with caution. (ABSTRACT TRUNCATED)

Amino Acid Sequence↗

[A comparison of the results of topographic EEG mapping with the data from a neurological examination and computed tomography of the brain].

The data of topographic EEG brain mapping were compared to neurological evidence and CT data in 6 patients with organic lesions (sequelae of vertebrobasilar ischemic stroke, brain atrophy, brain tumor). Cortical activity typical for these nosological entities appeared on the EEG maps. In 5 out of 6 patients foci of alpha- and delta-activity indicated the location of the lesion. The authors suggest that EEG brain mapping of the large number of patients with neural and mental diseases will provide insight into pathogenetic mechanisms of these diseases. The authors also think it necessary for patients undergoing EEG brain mapping to be examined neurologically.

Adult↗

Automated production of high density cosmid and YAC colony filters using a robotic workstation.

We report here on a system for automated preparation of high-density colony filters of arrayed libraries using the high density replicating system (HDR) for the Beckman Biomek 1000 robotic workstation. This system, consisting of a 96-pin tool, a sterilization station and controlling software, transfers samples from microplates onto target membranes in arrays up to 36 times the density of a 96-well microplate. The transfer operation can be completely automated with the addition of the Biomek Side Loader System, which consists of a robotic arm capable of transferring plates and filters between the Biomek working tablet and a storage area. Using the complete system, we are able to plate 32 replica filters (8 x 12 cm), each containing the clones from 16 different microplates (i.e., 1536 clones per filter), in a 16-h overnight run without any operator intervention. We describe conditions used for transfer of bacterial yeast colonies and fixation of DNA to the membranes, and we illustrate hybridization results obtained with cosmid and YAC filters.

Biotechnology↗

An evaluation of the application of the genetic algorithm to the problem of ordering genetic loci on human chromosomes using radiation hybrid data.

We consider the problem of ordering detectable genetic loci along a chromosome by minimizing the number of obligatory breaks that can be inferred from radiation hybrid data. The problem bears some resemblance to the travelling-salesman problem, for which genetic algorithms have been used with considerable success. We find that the results from other studies on closely related problems are not directly transferable, and although we did find a genetic algorithm that performed well in this application it would appear that this algorithm is highly sensitive to any changes in the problem. Moreover, a very simple stochastic algorithm performed almost as well as our much more complicated and computer-intensive genetic algorithm and it did so in a fraction of the time. While we do not dispute that genetic algorithms can work on large complicated problems, the various modifications and fine-tuning necessary for good performance tend to be highly problem specific and they are often only arrived at after an exhaustive exploration of possibilities. Thus, we would dispute any claim that genetic algorithms are robust in their form and range of applicability.

Algorithms↗

Ontologies for molecular biology.

Molecular biology has a communication problem. There are many databases using their own labels and categories for storing data objects and some using identical labels and categories but with a different meaning. A prominent example is the concept "gene" which is used with different semantics by major international genomic databases. Ontologies are one means to provide a semantic repository to systematically order relevant concepts in molecular biology and to bridge the different notions in various databases by explicitly specifying the meaning of and relation between the fundamental concepts in an application domain. Here, the upper level and a database branch of a prospective ontology for molecular biology (OMB) is presented and compared to other ontologies with respect to suitability for molecular biology (http:/(/)igd.rz-berlin.mpg.de/approximately www/oe/mbo.html).

Chromosome Mapping↗