Evolutionary Relationships of Major Histocompatibility Complex Class I Genes in Simian Primates

Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1897-1907
Author(s):  
Hiromi Sawai ◽  
Yoshi Kawamoto ◽  
Naoyuki Takahata ◽  
Yoko Satta
Keyword(s):  
Major Histocompatibility Complex ◽  
Distinct Group ◽  
Gene Organization ◽  
Class I ◽  
Phylogenetic Position ◽  
Specific Gene ◽  
New World Monkeys ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Histocompatibility Complex

Abstract New World monkeys (NWMs) occupy a critical phylogenetic position in elucidating the evolutionary process of major histocompatibility complex (MHC) class I genes in primates. From three subfamilies of Aotinae, Cebinae, and Atelinae, the 5′-flanking regions of 18 class I genes are obtained and phylogenetically examined in terms of Alu/LINE insertion elements as well as the nucleotide substitutions. Two pairs of genes from Aotinae and Atelinae are clearly orthologous to human leukocyte antigen (HLA) -E and -F genes. Of the remaining 14 genes, 8 belong to the distinct group B, together with HLA-B and -C, to the exclusion of all other HLA class I genes. These NWM genes are classified into four groups, designated as NWM-B1, -B2, -B3, and -B4. Of these, NWM-B2 is orthologous to HLA-B/C. Also, orthologous relationships of NWM-B1, -B2, and -B3 exist among different families of Cebidae and Atelidae, which is in sharp contrast to the genus-specific gene organization within the subfamily Callitrichinae. The other six genes belong to the distinct group G. However, a clade of these NWM genes is almost equally related to HLA-A, -J, -G, and -K, and there is no evidence for their orthologous relationships to HLA-G. It is argued that class I genes in simian primates duplicated extensively in their common ancestral lineage and that subsequent evolution in descendant species has been facilitated mainly by independent loss of genes.

scholarly journals Microrecombinations generate sequence diversity in the murine major histocompatibility complex: analysis of the Kbm3, Kbm4, Kbm10, and Kbm11 mutants.

1988 ◽  
Vol 8 (10) ◽  
pp. 4342-4352 ◽  
Author(s):  
J Geliebter ◽  
S G Nathenson
Keyword(s):  
Major Histocompatibility Complex ◽  
Complex Analysis ◽  
Sequence Diversity ◽  
Class I ◽  
Nucleotide Sequence Analysis ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Mouse Population ◽  
Histocompatibility Complex ◽  
Spontaneous Mutants

The mechanism that generates spontaneous mutants of the Kb histocompatibility gene was analyzed. Nucleotide sequence analysis of four mutant genes (Kbm3, Kbm4, Kbm10, and Kbm11) revealed that each mutant K gene contains clustered, multiple nucleotide substitutions. Hybridization analyses of parental B6 genomic DNA and cloned class I genes with mutant-specific oligonucleotide probes, followed by sequence analyses, have identified major histocompatibility complex class I genes in the K, D, and Tla regions (K1, Db, and T5, respectively) that contain the exact sequences as substituted into mutant Kb genes. These data provide evidence for the hypothesis that the mutant Kb genes are generated by a microrecombination (gene conversion) mechanism that results in the transfer of small DNA segments from class I genes of all four regions of the major histocompatibility complex (K, D, Qa, and Tla) to Kb. Many of the nucleotides substituted into the mutant Kb genes were identical to those found in other naturally occurring K alleles such as Kd. Thus, we propose that the accumulation of microrecombination products within the K genes of a mouse population is responsible for the high sequence diversity among H-2 alleles.

Gene organization of the quail major histocompatibility complex ( MhcCoja ) class I gene region

1999 ◽  
Vol 49 (5) ◽  
pp. 384-394 ◽  
Author(s):  
Takashi Shiina ◽  
Chiori Shimizu ◽  
Akira Oka ◽  
Yoshika Teraoka ◽  
Tadashi Imanishi ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Gene Organization ◽  
Class I ◽  
Gene Region ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
I Gene

Binding of multiple nuclear factors to the 5' upstream regulatory element of the murine major histocompatibility class I gene

1987 ◽  
Vol 7 (12) ◽  
pp. 4542-4548
Author(s):  
Y Shirayoshi ◽  
J Miyazaki ◽  
P A Burke ◽  
K Hamada ◽  
E Appella ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Protein Interactions ◽  
Regulatory Element ◽  
Negative Control ◽  
Class I ◽  
Control Element ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Mobility Shift ◽  
Histocompatibility Complex

Transcription of mouse major histocompatibility complex class I genes is controlled by the conserved class I regulatory element (CRE) in the 5' flanking region. The CRE, approximately 40 base pairs long, acts as a negative control element in undifferentiated F9 embryonal carcinoma cells which do not express the major histocompatibility complex genes. The same element, however, acts as a positive control element in cells expressing the genes at high levels. To investigate the molecular basis of the regulatory role of the CRE, we studied the binding of nuclear proteins to the CRE of the H-2Ld gene by gel mobility shift and methylation interference experiments. Nuclear extracts from L fibroblasts and LH8 T lymphocytes revealed three distinct factors that bind discrete sequences within the CRE. The three sequences correspond to the inverted and direct repeats within the CRE. In contrast, F9 extracts exhibited factor binding to only two of the three sequences and lack a major factor detected in the above two cell types. Protein-binding sites within each of the three sequences were identified by methylation interference experiments. These data were in full agreement with results obtained by a competition assay performed with a series of mutant oligonucleotides containing a few nucleotide substitutions in each of the three regions. The results illustrate complex DNA-protein interactions in which several independent proteins bind to overlapping sequences in the CRE in a cell type-specific fashion.

Microrecombinations generate sequence diversity in the murine major histocompatibility complex: analysis of the Kbm3, Kbm4, Kbm10, and Kbm11 mutants

1988 ◽  
Vol 8 (10) ◽  
pp. 4342-4352
Author(s):  
J Geliebter ◽  
S G Nathenson
Keyword(s):  
Major Histocompatibility Complex ◽  
Complex Analysis ◽  
Sequence Diversity ◽  
Class I ◽  
Nucleotide Sequence Analysis ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Mouse Population ◽  
Histocompatibility Complex ◽  
Spontaneous Mutants

The mechanism that generates spontaneous mutants of the Kb histocompatibility gene was analyzed. Nucleotide sequence analysis of four mutant genes (Kbm3, Kbm4, Kbm10, and Kbm11) revealed that each mutant K gene contains clustered, multiple nucleotide substitutions. Hybridization analyses of parental B6 genomic DNA and cloned class I genes with mutant-specific oligonucleotide probes, followed by sequence analyses, have identified major histocompatibility complex class I genes in the K, D, and Tla regions (K1, Db, and T5, respectively) that contain the exact sequences as substituted into mutant Kb genes. These data provide evidence for the hypothesis that the mutant Kb genes are generated by a microrecombination (gene conversion) mechanism that results in the transfer of small DNA segments from class I genes of all four regions of the major histocompatibility complex (K, D, Qa, and Tla) to Kb. Many of the nucleotides substituted into the mutant Kb genes were identical to those found in other naturally occurring K alleles such as Kd. Thus, we propose that the accumulation of microrecombination products within the K genes of a mouse population is responsible for the high sequence diversity among H-2 alleles.

scholarly journals Binding of multiple nuclear factors to the 5' upstream regulatory element of the murine major histocompatibility class I gene.

1987 ◽  
Vol 7 (12) ◽  
pp. 4542-4548 ◽  
Author(s):  
Y Shirayoshi ◽  
J Miyazaki ◽  
P A Burke ◽  
K Hamada ◽  
E Appella ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Protein Interactions ◽  
Regulatory Element ◽  
Negative Control ◽  
Class I ◽  
Control Element ◽  
Major Histocompatibility ◽  
Nucleotide Substitutions ◽  
Mobility Shift ◽  
Histocompatibility Complex

Transcription of mouse major histocompatibility complex class I genes is controlled by the conserved class I regulatory element (CRE) in the 5' flanking region. The CRE, approximately 40 base pairs long, acts as a negative control element in undifferentiated F9 embryonal carcinoma cells which do not express the major histocompatibility complex genes. The same element, however, acts as a positive control element in cells expressing the genes at high levels. To investigate the molecular basis of the regulatory role of the CRE, we studied the binding of nuclear proteins to the CRE of the H-2Ld gene by gel mobility shift and methylation interference experiments. Nuclear extracts from L fibroblasts and LH8 T lymphocytes revealed three distinct factors that bind discrete sequences within the CRE. The three sequences correspond to the inverted and direct repeats within the CRE. In contrast, F9 extracts exhibited factor binding to only two of the three sequences and lack a major factor detected in the above two cell types. Protein-binding sites within each of the three sequences were identified by methylation interference experiments. These data were in full agreement with results obtained by a competition assay performed with a series of mutant oligonucleotides containing a few nucleotide substitutions in each of the three regions. The results illustrate complex DNA-protein interactions in which several independent proteins bind to overlapping sequences in the CRE in a cell type-specific fashion.

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