Gene Conversion Events (gene + conversion_event)

Distribution by Scientific Domains


Selected Abstracts


The rate of terminal nucleotide loss from a telomere of the mosquito Anopheles gambiae

INSECT MOLECULAR BIOLOGY, Issue 1 2001
M. F. Walter
Abstract Using a single copy pUChsneo transgene insertion at the Anopheles gambiae 2L telomere, this chromosome end was monitored by genomic Southern blots for forty-four mosquito generations. During this time, the chromosome end lost terminal nucleotides at an apparently constant rate of 55 bp/generation, which can be accounted for by incomplete DNA replication and does not imply exonuclease activity. No telomere elongation events were detected, suggesting that a previously described gene conversion event at this transgene does not occur very frequently. Moreover, no evidence for elongation by transposable elements was found, as described in Drosophila melanogaster. These results are consistent with the proposal that gene conversion between complex terminal satellite repeats that are present at natural telomeres, represents the major telomere elongation mechanism in A. gambiae. Such recombination events between repetitive sequences would occur more frequently than between the single copy pUChsneo transgene on the 2L homologues. [source]


A novel HLA-A2 variant, A*9203, identified by sequence-based typing

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 1 2007
C.-C. Chu
Summary HLA-A*9203, found in Taiwan using sequence-based typing method, was identical to HLA-A*0207 in exon 3 but differed in exon 2 by five nucleotide substitutions at positions 240,282 corresponding to three amino acid changes at codons 62, 66 and 70. Since this substitution motif is also seen in A*11 and A*03, it is likely that a gene conversion event from A*11 or A*03 to a A*0207 backbone may have been the process used in generating HLA-A*9203. [source]


Recognition of HLA-A*0248 in a Chinese donor

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 3 2003
K. L. Yang
Summary HLA-A*0248, a rare allele originally found in an individual of Filipino background, was detected in a Chinese donor. We confirmed the novel sequence and analysed its serological reaction pattern. The exon 2 sequence of A*0248 was apparently generated in a gene conversion event with an A2 gene, receiving a sequence segment comprising codons 56 to 74 from an A*24 donor gene. Serological typing showed a clear-cut A2 reaction pattern, indicating that the three amino acid positions 62, 65 and 74, are probably not a critical part of the A2 epitope. Our typing experience also demonstrated that different typing technologies often complement each other in fine HLA typing. [source]


Dissecting initiation of gene conversion events

HUMAN MUTATION, Issue 8 2009
Maris Laan
No abstract is available for this article. [source]


Gene conversion causing human inherited disease: Evidence for involvement of non-B-DNA-forming sequences and recombination-promoting motifs in DNA breakage and repair,

HUMAN MUTATION, Issue 8 2009
Nadia Chuzhanova
Abstract A variety of DNA sequence motifs including inverted repeats, minisatellites, and the , recombination hotspot, have been reported in association with gene conversion in human genes causing inherited disease. However, no methodical statistically based analysis has been performed to formalize these observations. We have performed an in silico analysis of the DNA sequence tracts involved in 27 nonoverlapping gene conversion events in 19 different genes reported in the context of inherited disease. We found that gene conversion events tend to occur within (C+G)- and CpG-rich regions and that sequences with the potential to form non-B-DNA structures, and which may be involved in the generation of double-strand breaks that could, in turn, serve to promote gene conversion, occur disproportionately within maximal converted tracts and/or short flanking regions. Maximal converted tracts were also found to be enriched (P<0.01) in a truncated version of the ,-element (a TGGTGG motif), immunoglobulin heavy chain class switch repeats, translin target sites and several novel motifs including (or overlapping) the classical meiotic recombination hotspot, CCTCCCCT. Finally, gene conversions tend to occur in genomic regions that have the potential to fold into stable hairpin conformations. These findings support the concept that recombination-inducing motifs, in association with alternative DNA conformations, can promote recombination in the human genome. Hum Mutat 30:1,10, 2009. © 2009 Wiley-Liss, Inc. [source]


A novel mechanism for control of antigenic variation in the haemagglutinin gene family of Mycoplasma synoviae

MOLECULAR MICROBIOLOGY, Issue 4 2000
A. H. Noormohammadi
High-frequency phase and antigenic variation of homologous lipoprotein haemagglutinins has been seen in both the major avian mycoplasma pathogens, Mycoplasma synoviae and Mycoplasma gallisepticum. The expression and, hence, antigenic variation of the pMGA gene family (encoding these lipoproteins in M. gallisepticum) is controlled by variation in the length of a trinucleotide repeat motif 5, to the promoter of each gene. However, such a mechanism was not detected in preliminary observations on M. synoviae. Thus, the basis for control of variation in the vlhA gene family (which encodes the homologous haemagglutinin in M. synoviae) was investigated to enable comparison with its homologue in M. gallisepticum and with other lipoprotein gene families in mycoplasmas. The start point of transcription was identified 119 bp upstream of the initiation codon, but features associated with control of transcription in other mycoplasma lipoprotein genes were not seen. Comparison of three copies of vlhA revealed considerable sequence divergence at the 3, end of the gene, but conservation of the 5, end. Southern blot analysis of M. synoviae genomic DNA revealed that the promoter region and part of the conserved 5, coding sequence occurred as a single copy, whereas the remainder of the coding sequence occurred as multiple copies. A 9.7 kb fragment of the genome was found to contain eight tandemly repeated regions partially homologous to vlhA, all lacking the putative promoter region and the single-copy 5, end of vlhA, but extending over one of four distinct overlapping regions of the 3, coding sequence. Examination of sequential clones of M. synoviae established that unidirectional recombination occurs between the pseudogenes and the expressed vlhA, with duplication of pseudogene sequence and loss of the corresponding region previously seen in the expressed gene. Expression of the 5, end of two variants of the vlhA gene showed that they differed in their reaction with monoclonal antibodies specific for this region. These data suggest that the control of vlhA antigenic variation in M. synoviae is achieved by multiple gene conversion events using a repertoire of coding sequences to generate a chimeric expressed gene, with the greatest potential for variation generated in the region encoding the haemagglutinin. Thus, completely distinct mechanisms have been adopted to control antigenic variation in homologous gene families. [source]


Mutational analysis of SPANX genes in families with X-Linked prostate cancer

THE PROSTATE, Issue 8 2007
Natalay Kouprina
Abstract BACKGROUND Previous genetic linkage studies identified a locus for susceptibility to prostate cancer called HPCX at Xq27. The candidate region contains two clusters of SPANX genes. The first cluster called SPANX-A/D includes SPANX - A1, SPANX-A2, SPANX-B, SPANX-C, and SPANX-D; the second cluster called SPANX-N includes SPANX-N1, SPANX-N2, SPANX-N3, and SPANX-N4. The SPANX genes encode cancer-testis (CT) specific antigens. Previous studies identified SPANX-B and SPANX-D variants produced by gene conversion events, none of which are associated with X-linked prostate cancer. METHODS In this study we applied transformation-associated recombination cloning (TAR) in yeast to analyze sequence variations in SPANX - A1, SPANX - A2, and SPANX - C genes that are resided within large chromosomal duplications. A SPANX-N1/N4 cluster was analyzed by a routine PCR analysis. RESULTS None of the sequence variations in the coding regions of these genes is associated with susceptibility to prostate cancer. CONCLUSIONS Therefore, genetic variation in the SPANX genes is not the actual target variants explaining HPCX. However, it is possible that they play a modifying role in susceptibility to prostate cancer through complex recombinational interaction. Prostate 67: 820,828, 2007. © 2007 Wiley-Liss, Inc. [source]