Missed, Not Missing: Phylogenomic Evidence for the Existence of Avian FoxP3

Denyer, Michael P.; Pinheiro, Damilola; Garden, Oliver A.; Shepherd, Adrian J.

doi:10.1371/journal.pone.0150988

Cited by 20 publications

(15 citation statements)

References 67 publications

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“…Foxp3 gene was not found in most avian genomes [134], probably due to low quality of avian genomes. But recently, a Foxp3 like gene was evident in the genomes of two avian species [135]. In the context of MDV infection, a potential role of Treg cells has been indicated as the expression of IL-10 and CTLA-4 regulatory molecules increased on CD4 + T cells at 10 and 21 dpi, and this effect was more pronounced in the MDV-susceptible chicken lines [127,131].…”

Section: Regulatory T Cellsmentioning

confidence: 99%

Revisiting cellular immune response to oncogenic Marek’s disease virus: the rising of avian T-cell immunity

Yang

Dong

Hao

et al. 2020

Cell. Mol. Life Sci.

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Marek's disease virus (MDV) is a highly oncogenic alphaherpesvirus that causes deadly T-cell lymphomas and serves as a natural virus-induced tumor model in chickens. Although Marek's disease (MD) is well controlled by current vaccines, the evolution of MDV field viruses towards increasing virulence is concerning as a better vaccine to combat very virulent plus MDV is still lacking. Our understanding of molecular and cellular immunity to MDV and its immunopathogenesis has significantly improved, but those findings about cellular immunity to MDV are largely out-of-date, hampering the development of more effective vaccines against MD. T-cell-mediated cellular immunity was thought to be of paramount importance against MDV. However, MDV also infects macrophages, B cells and T cells, leading to immunosuppression and T-cell lymphoma. Additionally, there is limited information about how uninfected immune cells respond to MDV infection or vaccination, specifically, the mechanisms by which T cells are activated and recognize MDV antigens and how the function and properties of activated T cells correlate with immune protection against MDV or MD tumor. The current review revisits the roles of each immune cell subset and its effector mechanisms in the host immune response to MDV infection or vaccination from the point of view of comparative immunology. We particularly emphasize areas of research requiring further investigation and provide useful information for rational design and development of novel MDV vaccines.

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Section: Regulatory T Cellsmentioning

confidence: 99%

Revisiting cellular immune response to oncogenic Marek’s disease virus: the rising of avian T-cell immunity

Yang

Dong

Hao

et al. 2020

Cell. Mol. Life Sci.

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“…What drove the exceptional increase in regulatory complexity, in contrast to other genome duplication events? How do species that appear to have no homologues of Foxp3 [some birds (Andersen et al, ); possibly sea lamprey] operate dominant immune tolerance? Do they have a divergent form of the gene (Denyer et al, ), or an alternative mechanism has taken over its function? Is the LRR‐based somatic receptor diversity of jawless vertebrates the ancestral vertebrate condition, or did both LRR‐based and Ig/RAG‐based somatic diversity evolve after the split of jawless and jawed vertebrates? Is MHC restriction a fortuitous ‘complication’ in jawed vertebrates, or is this function necessary (inevitable) beyond some level of complexity or potency of Darwinian immunity? In the latter case, are jawless fish below this level, or do they have an analogous system to perform this function?…”

Section: The Origin Of Darwinian Immunity In Vertebratesmentioning

confidence: 99%

“…(6) How do species that appear to have no homologues of Foxp3 [some birds (Andersen et al, 2012); possibly sea lamprey] operate dominant immune tolerance? Do they have a divergent form of the gene (Denyer et al, 2016), or an alternative mechanism has taken over its function? (7) Is the LRR-based somatic receptor diversity of jawless vertebrates the ancestral vertebrate condition, or did both LRR-based and Ig/RAG-based somatic diversity evolve after the split of jawless and jawed vertebrates?…”

Section: (8) Outstanding Questions Of Darwinian Immunitymentioning

confidence: 99%

An evolutionary perspective on the systems of adaptive immunity

et al. 2017

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We propose an evolutionary perspective to classify and characterize the diverse systems of adaptive immunity that have been discovered across all major domains of life. We put forward a new function-based classification according to the way information is acquired by the immune systems: Darwinian immunity (currently known from, but not necessarily limited to, vertebrates) relies on the Darwinian process of clonal selection to 'learn' by cumulative trial-and-error feedback; Lamarckian immunity uses templated targeting (guided adaptation) to internalize heritable information on potential threats; finally, shotgun immunity operates through somatic mechanisms of variable targeting without feedback.We argue that the origin of Darwinian (but not Lamarckian or shotgun) immunity represents a radical innovation in the evolution of individuality and complexity, and propose to add it to the list of major evolutionary transitions. While transitions to higher-level units entail the suppression of selection at lower levels, Darwinian immunity re-opens cell-level selection within the multicellular organism, under the control of mechanisms that direct, rather than suppress, cell-level evolution for the benefit of the individual. From a conceptual point of view, the origin of Darwinian immunity can be regarded as the most radical transition in the history of life, in which evolution by natural selection has literally re-invented itself. Furthermore, the combination of clonal selection and somatic receptor diversity enabled a transition from limited to practically unlimited capacity to store information about the antigenic environment. The origin of Darwinian immunity therefore comprises both a transition in individuality and the emergence of a new information system -the two hallmarks of major evolutionary transitions.Finally, we present an evolutionary scenario for the origin of Darwinian immunity in vertebrates. We propose a revival of the concept of the 'Big Bang' of vertebrate immunity, arguing that its origin involved a 'difficult' (i.e. low-probability) evolutionary transition that might have occurred only once, in a common ancestor of all vertebrates. In contrast to the original concept, we argue that the limiting innovation was not the generation of somatic diversity, but the regulatory circuitry needed for the safe operation of amplifiable immune responses with somatically acquired targeting. Regulatory complexity increased abruptly by genomic duplications at the root of the vertebrate lineage, creating a rare opportunity to establish such circuitry. We discuss the selection forces that might have acted at the origin of the transition, and in the subsequent stepwise evolution leading to the modern immune systems of extant vertebrates.

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“…Therefore, it has been suggested that these genes were lost from avian genomes during the evolutionary process when microchromosomes were formed in the avian lineage [ 14 , 15 ]. However, technical difficulties in identification of some avian genes, due to their sequence characteristics and high sequence divergence, have been suggested as an alternative explanation [ 1 , 16 – 18 ]. Recently, the submission of a new version of the chicken genome assembly (Galgal5) revealed 1811 new protein-coding genes, however a fairly large number of genes belonging to clusters of genes showing conserved synteny in other species are still missing in the latest assembly [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Mapping of leptin and its syntenic genes to chicken chromosome 1p

et al. 2017

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BackgroundMisidentification of the chicken leptin gene has hampered research of leptin signaling in this species for almost two decades. Recently, the genuine leptin gene with a GC-rich (~70%) repetitive-sequence content was identified in the chicken genome but without indicating its genomic position. This suggests that such GC-rich sequences are difficult to sequence and therefore substantial regions are missing from the current chicken genome assembly.ResultsA radiation hybrid panel of chicken-hamster Wg3hCl2 cells was used to map the genome location of the chicken leptin gene. Contrary to our expectations, based on comparative genome mapping and sequence characteristics, the chicken leptin was not located on a microchromosome, which are known to contain GC-rich and repetitive regions, but at the distal tip of the largest chromosome (1p). Following conserved synteny with other vertebrates, we also mapped five additional genes to this genomic region (ARF5, SND1, LRRC4, RBM28, and FLNC), bridging the genomic gap in the current Galgal5 build for this chromosome region. All of the short scaffolds containing these genes were found to consist of GC-rich (54 to 65%) sequences comparing to the average GC-content of 40% on chromosome 1. In this syntenic group, the RNA-binding protein 28 (RBM28) was in closest proximity to leptin. We deduced the full-length of the RBM28 cDNA sequence and profiled its expression patterns detecting a negative correlation (R = − 0.7) between the expression of leptin and of RBM28 across tissues that expressed at least one of the genes above the average level. This observation suggested a local regulatory interaction between these genes. In adipose tissues, we observed a significant increase in RBM28 mRNA expression in breeds with lean phenotypes.ConclusionMapping chicken leptin together with a cluster of five syntenic genes provided the final proof for its identification as the true chicken ortholog. The high GC-content observed for the chicken leptin syntenic group suggests that other similar clusters of genes in GC-rich genomic regions are missing from the current genome assembly (Galgal5), which should be resolved in future assemblies of the chicken genome.Electronic supplementary materialThe online version of this article (doi:10.1186/s12863-017-0543-1) contains supplementary material, which is available to authorized users.

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Missed, Not Missing: Phylogenomic Evidence for the Existence of Avian FoxP3

Cited by 20 publications

References 67 publications

Revisiting cellular immune response to oncogenic Marek’s disease virus: the rising of avian T-cell immunity

Revisiting cellular immune response to oncogenic Marek’s disease virus: the rising of avian T-cell immunity

An evolutionary perspective on the systems of adaptive immunity

Mapping of leptin and its syntenic genes to chicken chromosome 1p

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