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At least 181 records · Page 10Linked to original sources
PubMed2007

Bone marrow-derived hemopoietic precursors commit to the T cell lineage only after arrival in the thymic microenvironment.

T lymphocytes develop in the thymus from hemopoietic precursors that commit to the T cell lineage under the influence of Notch signals. In this study, we show by single cell analyses that the most immature hemopoietic precursors in the adult mouse thymus are uncommitted and specify to the T cell lineage only after their arrival in the thymus. These precursors express high levels of surface Notch receptors and rapidly lose B cell potential upon the provision of Notch signals. Using a novel culture system with complexed, soluble Notch ligands that allows the titration of T cell lineage commitment, we find that these precursors are highly sensitive to both Delta and Jagged ligands. In contrast, their phenotypical and functional counterparts in the bone marrow are resistant to Notch signals that efficiently induce T cell lineage commitment in thymic precursors. Mechanistically, this is not due to differences in receptor expression, because early T lineage precursors, bone marrow lineage marker-negative, Sca-1-positive, c-Kit-positive and common lymphoid progenitor cells, express comparable amounts of surface Notch receptors. Our data demonstrate that the sensitivity to Notch-mediated T lineage commitment is stage-dependent and argue against the bone marrow as the site of T cell lineage commitment.

Animals↗
PubMed1999

Reduced folate carrier expression in acute lymphoblastic leukemia: a mechanism for ploidy but not lineage differences in methotrexate accumulation.

Methotrexate (MTX) is one of the most active and widely used agents for the treatment of acute lymphoblastic leukemia (ALL). To elucidate the mechanism for higher accumulation of MTX polyglutamates (MTX-PG) in hyperdiploid ALL and lower accumulation in T-lineage ALL, expression of the reduced folate carrier (RFC) was assessed by reverse transcription-polymerase chain reaction in ALL blasts isolated from newly diagnosed patients. RFC expression exhibited a 60-fold range among 29 children, with significantly higher expression in hyperdiploid B-lineage ALL (median, 11.3) compared with nonhyperdiploid ALL (median, 2.1; P <.0006), but no significant difference between nonhyperdiploid B-lineage and T-lineage ALL. Furthermore, mRNA levels of RFC (mapped by FISH to chromosome 21) were significantly related to chromosome 21 copy number (P =.0013), with the highest expression in hyperdiploid ALL blasts with 4 copies of chromosome 21. To assess the functional significance of gene copy number, MTX-PG accumulation was compared in ALL blasts isolated from 121 patients treated with either low-dose MTX (LDMTX; n = 60) or high-dose MTX (HDMTX; n = 61). After LDMTX, MTX-PG accumulation was highest in hyperdiploid B-lineage ALL with 4 copies of chromosome 21 (P =.011), but MTX-PG accumulation was not significantly related to chromosome 21 copy number after HDMTX (P =.24). These data show higher RFC expression as a mechanism for greater MTX accumulation in hyperdiploid B-lineage ALL and indicate that lineage differences in MTX-PG accumulation are not due to lower RFC expression in T-lineage ALL.

Carrier Proteins↗
PubMed1999

BSAP/Pax5A expression blocks survival and expansion of early myeloid cells implicating its involvement in maintaining commitment to the B-lymphocyte lineage.

Early B lymphopoiesis is marked by plasticity between the myeloid and B lineages. An attractive model for B-lineage development is that commitment to this lineage is partly determined by the ordered expression of genes that prohibit switching to the myeloid lineage. In this regard, whereas the role of the B-cell-specific transcription factor BSAP/Pax5A in regulating B-lymphoid-restricted gene expression has been well-established, its role in maintaining B-lineage commitment is unclear. Thus, BSAP/Pax5A was constitutively expressed in the multipotent EML cell line, which can be directed toward the myeloid lineage by culture with interleukin-3 (IL-3) and retinoic acid. EML cells expressing BSAP/Pax5A successfully acquired the myeloid lineage markers CD11b and F4/80 in response to IL-3 and retinoic acid, indicating differentiation to the myeloid lineage. However, these early myeloid cells failed to expand in culture with granulocyte-macrophage colony-stimulating factor and were directed instead toward an apoptotic pathway. In parallel, primary bone marrow stem cells transduced with retrovirus constitutively expressing BSAP/Pax5A began myeloid cell differentiation, but like the transformed EML model failed to expand in response to myeloid growth factors. These studies identify a role for BSAP/Pax5A in suppressing the response to myeloid growth factors, which may be a component of the regulatory processes that limit plasticity of early B-lymphoid progenitors.

B-Lymphocytes↗
PubMed2003

Genome duplication, subfunction partitioning, and lineage divergence: Sox9 in stickleback and zebrafish.

Teleosts are the most species-rich group of vertebrates, and a genome duplication (tetraploidization) event in ray-fin fish appears to have preceded this remarkable explosion of biodiversity. What is the relationship of the ray-fin genome duplication to the teleost radiation? Genome duplication may have facilitated lineage divergence by partitioning different ancestral gene subfunctions among co-orthologs of tetrapod genes in different teleost lineages. To test this hypothesis, we investigated gene expression patterns for Sox9 gene duplicates in stickleback and zebrafish, teleosts whose lineages diverged early in Euteleost evolution. Most expression domains appear to have been partitioned between Sox9a and Sox9b before the divergence of stickleback and zebrafish lineages, but some ancestral expression domains were distributed differentially in each lineage. We conclude that some gene subfunctions, as represented by lineage-specific expression domains, may have assorted differently in separate lineages and that these may have contributed to lineage diversification during teleost evolution.

Animals↗
PubMed2003

Two highly divergent ancient allelic lineages of the transporter associated with antigen processing (TAP) gene in Xenopus: further evidence for co-evolution among MHC class I region genes.

In the frog Xenopus, MHC class I antigen presentation and processing genes (the immunoproteasome LMP2 and LMP7 and the transporter TAP1 and TAP2) seem to be closely linked in a primordial organization. Two distinct lineages of class Ia and LMP7 loci were previously identified, thus strongly suggesting co-evolution among 'class I region' genes. We now show that the Xenopus MHC 'class I region' lies between class II and class III genes and we have isolated two distinct alleles at both the TAP1 and TAP2 loci. The alleles at each locus are remarkably divergent from each other and phylogenetic tree analysis revealed in both cases that they diverged from each other 60-100 million years ago (MYA). For lineage-frequency and linkage analysis, 25 wild-caught X. laevis and 16 X. tropicalis were examined. The two lineages were present in different frequencies for X. laevis and X. tropicalis. Nevertheless, in all cases, the LMP7, TAP1, and TAP2 lineages were found in a set comprising one of the two lineages. Furthermore, like the LMP7 lineages, the TAP lineages were detected in most Xenopus species that diverged from a common ancestor 80-100 MYA, suggesting that the 'class I region' biallelic lineages are under balancing selection.

Alleles↗
PubMed1994

Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms.

Analysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology-antibody-chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML-M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML-M2 and t(15;17) in AML-M3 were seen in granulocytic lineages only; t(14;18) in non-Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B-CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T-CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL-EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30-positive Reed-Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages.

Blast Crisis↗
PubMed1990

Undifferentiated acute leukemia and lineage infidelity (difficulties in classification and management).

The acute leukemias have been considered to represent a clonal expansion of a malignant transformed hematopoietic progenitor cell with adherence to either the myeloid or lymphoid lineage--"lineage fidelity." Lineage fidelity has been challenged by the demonstration of lineage switching or mixed-lineage leukemias. We describe a 7 year old male who presented with undifferentiated acute leukemia and nasopharyngeal and cervical masses. His blasts had the morphologic appearance of myeloblasts (FAB M1) and were positive solely for the myeloid antigen CD15. He entered a complete remission (CR) with acute nonlymphocytic leukemia therapy. At first relapse he had evidence of mixed-lineage leukemia with B-cell lymphoid and myeloid phenotypes. He again relapsed from a second CR with Burkitt-cell leukemia. Cytogenetic findings showed a consistent 14q+, 17p+ abnormality in the blasts and nasopharyngeal mass. The t(8;14) associated with Burkitt's lymphoma was found in the mass tissue only following passage in the nude mouse. Our patient demonstrates that limitations still exist in our ability to classify acute leukemia. That leukemic transformation occurred in a multipotential progenitor cell leading to undifferentiated leukemia at diagnosis and/or that chemotherapy can influence the genetic programs of leukemic cells leading to the evidence of mixed-lineage leukemia and lineage switching is supported.

Burkitt Lymphoma↗
PubMed1983

Developmental autonomy of muscle fine structure in muscle lineage cells of ascidian embryos.

We have observed ultrastructural features of muscle differentiation in the muscle lineage cells of cleavage-arrested whole embryos and partial embryos of ascidians. Whole embryos of Ciona intestinalis and Ascidia ceratodes were cleavage-arrested with cytochalasin B at the 8-cell stage and reared to an age equivalent to several hours after hatching; these embryos formed extensive myofilaments which were often further organized into myofibrils of different sizes and densities in the peripheral cytoplasm of the two muscle lineage blastomeres (B4.1 pair). Developing myofibrils in cleavage-arrested embryos resembled the muscle elements observed in normal hatched larvae, but were less uniformly organized. A similar development of myofilaments and myofibrils occurred in the muscle lineage cells of multicellular partial embryos reared to "hatching" age. These partial embryos resulted from the isolated muscle lineage pair (B4.1) of blastomeres of the 8-cell stage (Ciona and Ascidia), and from a muscle lineage blastomere pair (B5.2) isolated at the 16-cell stage (Ascidia). Muscle lineage cells in the partial embryos were readily identified by the dense aggregates of mitochondria in their cytoplasm. Taken together, these results from the two kinds of partial embryo effectively eliminate inductive interactions with embryonic tissues other than mesodermal as a necessary factor in the onset of self-differentiation in muscle lineage cells. The relative complexity of muscle phenotype expressed in cleavage-arrested and partial embryos attests to an unusually strong developmental autonomy in the ascidian muscle lineages. This autonomy lends further support to the theory that a localized and segregated egg cytoplasmic determinant is responsible for larval muscle development in ascidian embryos.

Animals↗
PubMed1991

An evolutionary change in the muscle lineage of an anural ascidian embryo is restored by interspecific hybridization with a urodele ascidian.

Anural ascidians do not develop into a conventional tailed larva with differentiated muscle cells, however, embryos of some anural ascidian species retain the ability to express acetylcholinesterase (AChE) in a vestigial muscle cell lineage. This study examines the number of AChE-positive cells that develop in the anural ascidian Molgula occulta relative to that in the closely related urodele (tailed) species, Molgula oculata. Histochemical assays showed that M. oculata embryos develop 36 to 38 AChE-positive cells, consistent with the number of tail muscle cells expressed in other urodele ascidians. In contrast, M. occulta embryos develop a mean of only 20 AChE-positive cells in their vestigial muscle lineage. Cleavage-arrested embryos of the anural species express AChE only in B-line blastomeres, showing that the vestigial muscle lineage cells are derived from the primary muscle lineage. Less than the expected number of AChE-positive B-line cells develop in cleavage-arrested anural embryos, however, implying that the allocation of primary muscle lineage cells is decreased. Eggs of the anural species can be fertilized with sperm of the urodele species resulting in the development of some larvae that contain a short tail and/or a brain melanocyte, specific features of urodele larvae. The typical urodele number of AChE-positive cells is restored in some of these hybrid embryos. Both primary and secondary muscle lineages are restored because cleavage-arrested hybrid embryos develop more AChE-positive cells in the B-line blastomeres and supernumerary AChE-positive cells in the A-line blastomeres. Hybrid embryos that develop the urodele complement of AChE-positive cells also form a tail and/or a brain melanocyte showing that restoration of muscle lineage cells is coupled to the development of other urodele features. AChE expression occurred in anural embryos with disorganized or dissociated blastomeres, indicating that AChE expression is determined autonomously. It is concluded that an evolutionary change in the allocation of larval muscle lineage cells occurs during development of the anural ascidian M. occulta which can be restored by interspecific hybridization with the urodele ascidian M. oculata.

Acetylcholinesterase↗
PubMed1989

Cell lineage markers in premalignant and malignant colonic mucosa.

Normal colonic epithelial cells consist of several cell types or lineages that are thought to arise from a common stem cell precursor. Neoplastic transformation may occur at different stages in the differentiation of a colonic stem cell to produce tumors that may retain characteristic cell lineage phenotypes. In this study, immunohistochemical techniques were used to identify cell lineage-related markers in fetal, normal, hyperplastic, adenomatous, and cancerous colonic tissue. These markers consisted of secretory component (columnar cells), a purified mucin antigen (mucous or goblet cells), chromogranin A (enteroendocrine cells), lysozyme (Paneth cells), and carcinoembryonic antigen (panepithelial cell marker). Colonic neoplasms, like normal mucosa, predominantly expressed the markers of columnar and goblet cell lineages. Chromogranin A was expressed in a small population of cells in most normal and fetal colonic crypts. Chromogranin A reactive cells were found in 55% of hyperplastic polyps, 31% of adenomatous polyps, and 33% of carcinomas. Lysozyme reactivity was rare in fetal, normal, and hyperplastic specimens, but was present in 86% of adenomas and 40% of carcinomas. Of 42 primary carcinomas, 9% were "pluripotent" and expressed markers of all four cell lineages. In addition to columnar and goblet cell markers, 7% expressed both enteroendocrine and Paneth cell markers, 17% expressed enteroendocrine cell markers, and 24% expressed Paneth cell markers. Two cases (5%) lacked expression of any of the cell lineage markers. The remainder expressed only columnar and goblet cell markers. The markers used in this study appear to identify the major cell lineages of fetal and normal colonic epithelium and can be used to delineate the altered cell lineage phenotypes in premalignant and malignant colonic mucosa.

Biomarkers, Tumor↗
PubMed1981

Mutations that lead to reiterations in the cell lineages of C. elegans.

Cells in the nematode Caenorhabditis elegans arise from invariant cell lineages. Mutations in two genes, unc-86 and lin-4, alter multiple and mutually exclusive sets of these lineages. In these mutants, particular cells repeat division patterns normally associated with their parental or grandparental progenitors. The effects of unc-86 are highly specific, altering in equivalent ways the lineages of three post-embryonic neuroblasts that in the wild-type undergo similar division patterns. The effects of lin-4 are more varied, resulting in a number of types of lineage reiterations as well as in supernumerary molts and the continued synthesis of larval-specific cuticle. The reiteration of a given cell division or pattern of cell divisions leads to the repeated generation of cells indistinguishable (by both light and electron microscopy) from those produced after the same division or pattern of cell divisions in the wild-type. This correlation between lineage history and cell fate suggests that in C. elegans a particular sequence of cell divisions may be necessary for the generation of a particular cell type. Reiterative lineages, often referred to as stem cell lineages, may be basic to the development of nematodes and other organisms. We suggest that the wild-type unc-86 and lin-4 genes act to modify latent reiterative cell lineages, which are revealed when the activity of one of these genes is eliminated.

Animals↗
PubMed2005

A porcine G9 rotavirus strain shares neutralization and VP7 phylogenetic sequence lineage 3 characteristics with contemporary human G9 rotavirus strains.

Of five globally important VP7 (G) serotypes (G1-4 and 9) of group A rotaviruses (the single most important etiologic agents of infantile diarrhea worldwide), G9 continues to attract considerable attention because of its unique natural history. Serotype G9 rotavirus was isolated from a child with diarrhea first in the United States in 1983 and subsequently in Japan in 1985. Curiously, soon after their detection, G9 rotaviruses were not detected for about a decade in both countries and then reemerged in both countries in the mid-1990s. Unexpectedly, however, such reemerged G9 strains were distinct genetically and molecularly from those isolated in the 1980s. Thus, the origin of the reemerged G9 viruses remains an enigma. Sequence analysis has demonstrated that the G9 rotavirus VP7 gene belongs to one of at least three phylogenetic lineages: lineage 1 (strains isolated in the 1980s in the United States and Japan), lineage 2 (strains first isolated in 1986 and exclusively in India thus far), and lineage 3 (strains that emerged/reemerged in the mid-1990s). Currently, lineage 3 G9 viruses are the most frequently detected G9 strains globally. We characterized a porcine rotavirus (A2 strain) isolated in the United States that was known to belong to the P[7] genotype but had not been serotyped by neutralization. The A2 strain was found to bear serotype G9 and P9 specificities as well as NSP4 [B] and subgroup I characteristics. By VP7-specific neutralization, the porcine G9 strain was more closely related to lineage 3 viruses than to lineage 1 or 2 viruses. Furthermore, by sequence analysis, the A2 VP7 was shown to belong to lineage 3 G9. These findings raise intriguing questions regarding possible explanations for the emergence of variations among the G9 strains.

Amino Acid Sequence↗
PubMed2003

An SNP-based PCR assay to differentiate between Listeria monocytogenes lineages derived from phylogenetic analysis of the sigB gene.

The alternative sigma factor sigB gene is involved in the stress response regulation of Listeria monocytogenes, and contributes towards growth and survival in adverse conditions. This gene was examined to determine if it could be a useful indicator of lineage differentiation, similar to the established method based on ribotyping. The sigB sequence was resolved in four local L. monocytogenes strains and the phylogenetic relationship among these, and a further 21 sigB gene sequences from strains of different serotype and lineage including two Listeria innocua strains, obtained from the GenBank database were determined. The sigB nucleotide sequences of these 25 Listeria strains were then examined for single nucleotide polymorphic (SNP) sites that could differentiate between the three lineages. Based on nucleotide sequences L. monocytogenes lineage I/serotype 1/2b and 4b clustered together, lineage II/serotype 1/2a and 1/2c strains clustered together, lineage III/serotypes 4a and 4c strains clustered together and L. innocua strains clustered together as an outgroup. SNPs differentiating the three lineages were identified. Individual allele-specific PCR reactions based on these polymorphisms were successful in grouping known and a further 37 local L. monocytogenes isolates into the three lineages.

Alleles↗
PubMed2003

Evolving lineages of Symbiodinium-like dinoflagellates based on ITS1 rDNA.

Symbiodinium-like dinoflagellates have been shown to be a diverse group of endosymbionts that associate mutualistically with many kinds of coral reef dwellers, including cnidarians, molluscs, and protists. A high number of genetically ITS types of symbionts have been reported to date. However, whether these recently identified Symbiodinium ITS types indeed represent independent evolutionary lineages is still unsettled. Here I tested the null hypothesis that certain group of symbionts sampled from different geographical locations are derived from a single evolutionary lineage using a nested clade analysis (NCA). I analyzed a total of 174 ITS1 sequences from GenBank and pooled them into 74 ITS1 distinct haplotypes. Using these haplotypes, the statistical parsimony criterion produced 23 independent network trees, each one corresponding to a genetically independent evolving lineage. Some of these lineages revealed certain degree of specificity with some host groups at least at the phylum level. Within the previously described 28S-rDNA phylotype A, five ITS1 lineages were resolved. Phylotypes B and C resolved each in two ITS1 lineages. The highest ITS1 symbiont diversity was observed within the phylotype F, in which 11 lineages were resolved. Moreover, most of these lineages were associated uniquely with protist hosts from the group of foraminiferans. Here it is suggested that this high genetic diversity of endosymbionts associated with foraminiferans is linked with the evolution of soritacean foraminifera, which seems to have been driven by endosymbiosis. Lastly, the absence of genetic recombination presented in this study, suggest a lack of hybridisation at least among the major 28S-rDNA phylotypes within Symbiodinium-like dinoflagellates. This supports highly the idea that these phylotypes are indeed independent evolutionary units, which should be considered at least as different species. Whether they belong to the same genus or to different higher taxa still needs to be revised.

Animals↗
PubMed2003

Maintenance of aphid clonal lineages: images of immortality?

Artificial cloning and ancient asexuals have impacted upon both scientific and lay thinking in applied and theoretical fields as diverse as medicine and evolution. Hence, this is an opportune time to promote debate and discussion on what maintains a clonal lineage. The genetic fidelity of a clone has been discussed in detail elsewhere [Genet. Res. 79 (2002) 1; Biol. J. Linnean Soc. 79 (2003) 3]. In this paper, we focus on the lineage integrity (=longevity), or physiological lifespan of a clone with respect to senesce in relation to factors controlling telomere functioning. Aspects of cell line research pertinent to eukaryotic clonal lineages are discussed and, in particular, we try to extrapolate aspects of this research and apply it to apomictic (=mitotic) aphid lineages to suggest how they may be maintained. Analogies are made between single cells and individual aphids that senescence through a generation, whilst the respective lineages persist for finite periods, unless that is, compensatory mechanisms have evolved allowing immortality in the one and ancient asexuality in the other. Such comparison may allow fresh insights into the mechanisms of clonal lineage maintenance and evolution. We hypothesise that: (1). the cause of extinction in eukaryotic clonal lineages is due to deleterious effects on key regions of the genome, the chromosomal telomere being one such site; (2). recombination acts as a common mechanism to reset telomere functioning, perhaps more fundamental than its utility to reduce genetic load and maintain adaptability; and (3). ancient lineages persist through time as a function of group-specific compensatory mechanisms that maintain telomere integrity.

Aging↗
PubMed2004

Epidemics of two Victoria and Yamagata influenza B lineages in Yamagata, Japan.

We attempted to predict epidemics of influenza B, focusing on B/Victoria/2/87-like (V) and B/Yamagata/16/88-like (Y) lineages, in Yamagata, Japan. We collected 9624 nasopharyngeal swabs for virus isolation from patients with respiratory infections between 1996 and 2003 and 237 sera for seroepidemiological analysis by haemagglutination-inhibition test in 2001. We isolated 424 V-lineage and 246 Y-lineage viruses during the study period. Three herald viruses in the 2000--2001 season enabled us to predict a V-lineage epidemic in the following season. However, another V-lineage epidemic occurred in the 2002--2003 season, although we caught four herald Y-lineage viruses, whose antigenic drift was suggested by seroepidemiological study, at the end of the previous season. Since the epidemiology of the two influenza B lineages remains unclear, a careful watch should be kept on these lineages in order to provide effective public-health strategies against future epidemics.

Adolescent↗
PubMed2025

Doblin: inferring dominant clonal lineages from high-resolution DNA barcoding time series.

MOTIVATION: The lineage dynamics and history of cells in a population reflect the interplay of evolutionary forces they experience, including mutation, drift, and selection. When the population is polyclonal, lineage dynamics also manifest the extent of clonal competition among co-existing mutational variants. If the population exists in a community of other species, the lineage dynamics could also reflect the population's ecological interaction with the rest of the community. Recent advances in high-resolution lineage tracking via DNA barcoding, coupled with next-generation sequencing of bacteria, yeast, and mammalian cells, allow for precise quantification of clonal dynamics in these organisms. RESULTS: In this work, we introduce Doblin, an R suite for identifying dominant barcode lineages based on high-resolution lineage tracking data. We first benchmarked Doblin's accuracy using lineage data from evolutionary simulations, showing that it recovers the clones' identity and relative fitness in the simulation. Next, we applied Doblin to analyze clonal dynamics in laboratory evolutions of Escherichia coli populations undergoing antibiotic treatment and in colonization experiments of the gut microbial community. Doblin's versatility allows it to be applied to lineage time-series data across different experimental setups. AVAILABILITY AND IMPLEMENTATION: Doblin is available on CRAN (https://CRAN.R-project.org/package=doblin) and Github (https://github.com/dagagf/doblin).

DNA Barcoding, Taxonomic↗
PubMed1998

Molecular evolution of two lineages of L1 (LINE-1) retrotransposons in the california mouse, Peromyscus californicus.

The large number of L1 [long interspersed elements (LINE)-1] sequences found in the genome is due to the insertion of copies of the retrotransposon over evolutionary time. The majority of copies appear to be replicates of a few active, or "master" templates. A continual replacement of master templates over time gives rise to lineages distinguishable by their own unique set of shared-sequence variants. A previous analysis of L1 sequences in deer mice, Peromyscus maniculatus and P. leucopus, revealed two active L1 lineages, marked by different rates of evolution, whose most recent common ancestor predates the expansion of the Peromyscus species. Here we exploit lineage-specific, shared-sequence variants to reveal a paucity of Lineage 2 sequences in at least one species, P. californicus. The dearth of Lineage 2 copies in P. californicus suggests that Lineage 2 may have been unproductive until after the most recent common ancestor of P. californicus and P. maniculatus. We also show that Lineage 1 appears to have a higher rate of evolution in P. maniculatus relative to either P. californicus or P. leucopus. As a phylogenetic tool, L1 lineage-specific variants support a close affinity between P. californicus and P. eremicus relative to the other species examined.

Animals↗