Evidence for the loss of plasminogen receptor KT gene in chicken

Sharma, Sandhya; Shinde, Sagar Sharad; Teekas, Lokdeep; Vijay, Nagarjun

doi:10.1007/s00251-020-01186-2

Cited by 9 publications

(12 citation statements)

References 53 publications

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“…Together, such a distribution of plasminogen and its major activators would explain the ability of CK/BE/1940/19 to replicate systemically including neuronal tissues despite a monobasic HACS. Beside that the most information about plasminogen distribution and function are derived from mammals, the plasminogen system is mostly conserved in chordates [74] and there are strong indications that most of them are also basically applicable for avian species, here chickens [75][76][77]. In addition, endothelial cells are highly active plasminogen producers, secreting plasminogen but also the membrane-bound uPA-receptor that mediates plasminogen and uPA colocalization on the membrane surface [78][79][80].…”

Section: Discussionmentioning

confidence: 99%

Neuraminidase-associated plasminogen recruitment enables systemic spread of natural avian Influenza viruses H3N1

et al. 2021

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Repeated outbreaks due to H3N1 low pathogenicity avian influenza viruses (LPAIV) in Belgium were associated with unusually high mortality in chicken in 2019. Those events caused considerable economic losses and prompted restriction measures normally implemented for eradicating high pathogenicity avian influenza viruses (HPAIV). Initial pathology investigations and infection studies suggested this virus to be able to replicate systemically, being very atypical for H3 LPAIV. Here, we investigate the pathogenesis of this H3N1 virus and propose a mechanism explaining its unusual systemic replication capability. By intravenous and intracerebral inoculation in chicken, we demonstrate systemic spread of this virus, extending to the central nervous system. Endoproteolytic viral hemagglutinin (HA) protein activation by either tissue-restricted serine peptidases or ubiquitous subtilisin-like proteases is the functional hallmark distinguishing (H5 or H7) LPAIV from HPAIV. However, luciferase reporter assays show that HA cleavage in case of the H3N1 strain in contrast to the HPAIV is not processed by intracellular proteases. Yet the H3N1 virus replicates efficiently in cell culture without trypsin, unlike LPAIVs. Moreover, this trypsin-independent virus replication is inhibited by 6-aminohexanoic acid, a plasmin inhibitor. Correspondingly, in silico analysis indicates that plasminogen is recruitable by the viral neuraminidase for proteolytic activation due to the loss of a strongly conserved N-glycosylation site at position 130. This mutation was shown responsible for plasminogen recruitment and neurovirulence of the mouse brain-passaged laboratory strain A/WSN/33 (H1N1). In conclusion, our findings provide good evidence in natural chicken strains for N1 neuraminidase-operated recruitment of plasminogen, enabling systemic replication leading to an unusual high pathogenicity phenotype. Such a gain of function in naturally occurring AIVs representing an established human influenza HA-subtype raises concerns over potential zoonotic threats.

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Section: Discussionmentioning

confidence: 99%

Neuraminidase-associated plasminogen recruitment enables systemic spread of natural avian Influenza viruses H3N1

et al. 2021

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“…Recurrent gene loss events following relaxed selective constraint in various other lineages have also been documented (Schneider et al, 2019; Sharma and Hiller, 2018; Valente et al, 2020). Loss of genes in the Galliform lineage while being intact in the Anseriformes lineage has been linked to differences in the immune response of these clades (Barber et al, 2010; S. Sharma et al, 2020). The COA1/MITRAC15 gene is not known to have any obvious immune functions, and its loss in Galliform birds appears to be a consequence of relaxed selection on the OXPHOS pathway.…”

Section: Discussionmentioning

confidence: 99%

“…We used a previously published 5-pass strategy to verify gene loss events (S. Sharma et al, 2020). Briefly, to verify the correctness of the genome assembly nucleotide sequence, we used the COA1/MITRAC15 gene sequence of multiple species as a query for a blastn search of the raw short-read database.…”

Section: Methodsmentioning

confidence: 99%

Recurrent erosion ofCOA1/MITRAC15demonstrates gene dispensability in oxidative phosphorylation

Sharma

Teekas

et al. 2021

Preprint

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Skeletal muscle fibers rely upon either oxidative phosphorylation or glycolytic pathway to achieve muscular contractions that power mechanical movements. Species with energy-intensive adaptive traits that require sudden bursts of energy have a greater dependency on fibers that use the glycolytic pathway. Glycolytic fibers have decreased reliance on OXPHOS and lower mitochondrial content compared to oxidative fibers. Hence, we hypothesized that adaptive gene loss might have occurred within the OXPHOS pathway in lineages that largely depend on glycolytic fibers. The protein encoded by the COA1/MITRAC15 gene with conserved orthologs found in budding yeast to humans promotes mitochondrial translation. We show that gene disrupting mutations have accumulated within the COA1/MITRAC15 gene in the cheetah, several species of galliforms, and rodents. The genomic region containing COA1/MITRAC15 is a well-established evolutionary breakpoint region in mammals. Careful inspection of genome assemblies of closely related species of rodents and marsupials suggests two independent COA1/MITRAC15 gene loss events co-occurring with chromosomal rearrangements. Besides recurrent gene loss events, we document changes in COA1/MITRAC15 exon structure in primates and felids. The detailed evolutionary history presented in this study reveals the intricate link between skeletal muscle fiber composition and dispensability of the chaperone-like role of the COA1/MITRAC15 gene.

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“…Recent molecular genetic studies have shown that several genes supposedly involved in the endocrine system, including those involved in insulin sensitivity, are missing in the bird genome [37][38][39][40][41].…”

Section: Establishment Of Insulin Resistancementioning

confidence: 99%

Bird evolution by insulin resistance

Satoh

2021

Trends in Endocrinology & Metabolism

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Drift of oxygen concentrations in the atmosphere was one of the main drivers of the evolution of vertebrates. The drop in oxygen concentrations at the Permian-Triassic (PT) boundary may have been the biggest challenge to vertebrates. This hypoxic condition forced theropods to lose certain genes to maximize their efficiency of oxygen usage. Recent studies show that omentin and insulin-sensitive glucose transporter 4 (GLUT4) are missing in the bird genome. Since these gene products play essential roles in maintaining insulin sensitivity, this loss forced theropods to become insulin resistant. Insulin resistance may have been the key to allowing theropods to become hyperathletic under hypoxic conditions and to outcompete mammals during the Triassic period. A second challenge was the gradual increase in oxygen concentrations during the late Jurassic, Cretaceous, and Tertiary periods when reactive oxygen species (ROS) leakage from mitochondria became a problem. Since the simplest solution was the expansion of body size, some theropods became bigger to reduce ROS leakage per volume. Another solution was the development of a constitutively active countermeasure against ROS. A recent study shows that Neoaves have constitutively active nuclear factor erythroid 2-related factor 2 (NRF2) due to deletion of the C-terminal part of the KEAP1 protein, thus allowing Neoaves to express antioxidant enzymes to overcome ROS leakage.

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Evidence for the loss of plasminogen receptor KT gene in chicken

Cited by 9 publications

References 53 publications

Neuraminidase-associated plasminogen recruitment enables systemic spread of natural avian Influenza viruses H3N1

Neuraminidase-associated plasminogen recruitment enables systemic spread of natural avian Influenza viruses H3N1

Recurrent erosion ofCOA1/MITRAC15demonstrates gene dispensability in oxidative phosphorylation

Bird evolution by insulin resistance

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