scholarly journals How to make a rodent giant: Genomic basis and tradeoffs of gigantism in the capybara, the world’s largest rodent

2020 ◽  
Author(s):  
Santiago Herrera-Álvarez ◽  
Elinor Karlsson ◽  
Oliver A Ryder ◽  
Kerstin Lindblad-Toh ◽  
Andrew J Crawford
Keyword(s):  
Body Size ◽  
Draft Genome ◽  
Large Body ◽  
Comparative Genomic ◽  
Specific Gene ◽  
Large Body Size ◽  
Synonymous Mutations ◽  
Intragenomic Conflict ◽  
Genome Wide ◽  
A Genome

Abstract Gigantism results when one lineage within a clade evolves extremely large body size relative to its small-bodied ancestors, a common phenomenon in animals. Theory predicts that the evolution of giants should be constrained by two tradeoffs. First, because body size is negatively correlated with population size, purifying selection is expected to be less efficient in species of large body size, leading to increased mutational load. Second, gigantism is achieved through generating a higher number of cells along with higher rates of cell proliferation, thus increasing the likelihood of cancer. To explore the genetic basis of gigantism in rodents and uncover genomic signatures of gigantism-related tradeoffs, we assembled a draft genome of the capybara (Hydrochoerus hydrochaeris), the world’s largest living rodent. We found that the genome-wide ratio of non-synonymous to synonymous mutations (ω) is elevated in the capybara relative to other rodents, likely caused by a generation-time effect and consistent with a nearly-neutral model of molecular evolution. A genome-wide scan for adaptive protein evolution in the capybara highlighted several genes controlling post-natal bone growth regulation and musculoskeletal development, which are relevant to anatomical and developmental modifications for an increase in overall body size. Capybara-specific gene-family expansions included a putative novel anticancer adaptation that involves T cell-mediated tumor suppression, offering a potential resolution to the increased cancer risk in this lineage. Our comparative genomic results uncovered the signature of an intragenomic conflict where the evolution of gigantism in the capybara involved selection on genes and pathways that are directly linked to cancer.

scholarly journals How to make a rodent giant: Genomic basis and tradeoffs of gigantism in the capybara, the world’s largest rodent

2018 ◽  
Author(s):  
Santiago Herrera-Álvarez ◽  
Elinor Karlsson ◽  
Oliver A. Ryder ◽  
Kerstin Lindblad-Toh ◽  
Andrew J. Crawford
Keyword(s):  
Cell Proliferation ◽  
Body Size ◽  
T Cell ◽  
Growth Regulation ◽  
Large Body ◽  
Mutation Load ◽  
Large Body Size ◽  
Genome Wide ◽  
A Genome ◽  
Cancer Suppression

AbstractGigantism is the result of one lineage within a clade evolving extremely large body size relative to its small-bodied ancestors, a phenomenon observed numerous times in animals. Theory predicts that the evolution of giants should be constrained by two tradeoffs. First, because body size is negatively correlated with population size, purifying selection is expected to be less efficient in species of large body size, leading to a genome-wide elevation of the ratio of non-synonymous to synonymous substitution rates (dN/dS) or mutation load. Second, gigantism is achieved through higher number of cells and higher rates of cell proliferation, thus increasing the likelihood of cancer. However, the incidence of cancer in gigantic animals is lower than the theoretical expectation, a phenomenon referred to as Peto’s Paradox. To explore the genetic basis of gigantism in rodents and uncover genomic signatures of gigantism-related tradeoffs, we sequenced the genome of the capybara, the world’s largest living rodent. We found that dN/dS is elevated genome wide in the capybara, relative to other rodents, implying a higher mutation load. Conversely, a genome-wide scan for adaptive protein evolution in the capybara highlighted several genes involved in growth regulation by the insulin/insulin-like growth factor signaling (IIS) pathway. Capybara-specific gene-family expansions included a putative novel anticancer adaptation that involves T cell-mediated tumor suppression, offering a potential resolution to Peto’s Paradox in this lineage. Gene interaction network analyses also revealed that size regulators function simultaneously as growth factors and oncogenes, creating an evolutionary conflict. Based on our findings, we hypothesize that gigantism in the capybara likely involved three evolutionary steps: 1) Increase in body size by cell proliferation through the ISS pathway, 2) coupled evolution of growth-regulatory and cancer-suppression mechanisms, possibly driven by intragenomic conflict, and 3) establishment of the T cell-mediated tumor suppression pathway as an anticancer adaptation. Interestingly, increased mutation load appears to be an inevitable outcome of an increase in body size.Author SummaryThe existence of gigantic animals presents an evolutionary puzzle. Larger animals have more cells and undergo exponentially more cell divisions, thus, they should have enormous rates of cancer. Moreover, large animals also have smaller populations making them vulnerable to extinction. So, how do gigantic animals such as elephants and blue whales protect themselves from cancer, and what are the consequences of evolving a large size on the ‘genetic health’ of a species? To address these questions we sequenced the genome of the capybara, the world’s largest rodent, and performed comparative genomic analyses to identify the genes and pathways involved in growth regulation and cancer suppression. We found that the insulin-signaling pathway was involved in the evolution of gigantism in the capybara. We also found a putative novel anticancer mechanism mediated by the detection of tumors by T-cells, offering a potential solution to how capybaras mitigated the tradeoff imposed by cancer. Furthermore, we show that capybara genome harbors a higher proportion of slightly deleterious mutations relative to all other rodent genomes. Overall, this study provides insights at the genomic level into the evolution of a complex and extreme phenotype, and offers a detailed picture of how the evolution of a giant body size in the capybara has shaped its genome.

A new species of the subgenus Scheloribates (Topobates) (Acari: Oribatida: Scheloribatidae) from Panama

2020 ◽  
Vol 29 (2) ◽  
pp. 278-283
Author(s):  
S.G. Ermilov
Keyword(s):  
New Species ◽  
Body Size ◽  
Leaf Litter ◽  
Related Species ◽  
Large Body ◽  
Oribatid Mite ◽  
Neotropical Region ◽  
Large Body Size ◽  
First Time ◽  
A New Species

The oribatid mite subgenus Scheloribates (Topobates) Grandjean, 1958, is recorded from the Neotropical region for the first time. A new species of this subgenus is described from the leaf litter collected in Cayo Agua Island, Panama. Scheloribates (Topobates) panamaensis sp. nov. differs from its related species by the very large body size and presence of a strong ventrodistal process on the leg femora II–IV.

scholarly journals Atmospheric Hypoxia Limits Selection for Large Body Size in Insects

PLoS ONE ◽  
2009 ◽  
Vol 4 (1) ◽  
pp. e3876 ◽  
Author(s):  
C. Jaco Klok ◽  
Jon F. Harrison
Keyword(s):  
Body Size ◽  
Large Body ◽  
Large Body Size ◽  
Selection For

scholarly journals Genome assembly of the JD17 soybean provides a new reference genome for Comparative genomics

2021 ◽  
Author(s):  
Xinxin Yi ◽  
Jing Liu ◽  
Shengcai Chen ◽  
Hao Wu ◽  
Min Liu ◽  
...  
Keyword(s):  
Nitrogen Fixation ◽  
Genome Assembly ◽  
Reference Genome ◽  
De Novo ◽  
Genomic Analysis ◽  
Comparative Genomic ◽  
High Quality ◽  
Genome Wide ◽  
A Genome ◽  
Cultivated Soybean

Cultivated soybean (Glycine max) is an important source for protein and oil. Many elite cultivars with different traits have been developed for different conditions. Each soybean strain has its own genetic diversity, and the availability of more high-quality soybean genomes can enhance comparative genomic analysis for identifying genetic underpinnings for its unique traits. In this study, we constructed a high-quality de novo assembly of an elite soybean cultivar Jidou 17 (JD17) with chromsome contiguity and high accuracy. We annotated 52,840 gene models and reconstructed 74,054 high-quality full-length transcripts. We performed a genome-wide comparative analysis based on the reference genome of JD17 with three published soybeans (WM82, ZH13 and W05) , which identified five large inversions and two large translocations specific to JD17, 20,984 - 46,912 PAVs spanning 13.1 - 46.9 Mb in size, and 5 - 53 large PAV clusters larger than 500kb. 1,695,741 - 3,664,629 SNPs and 446,689 - 800,489 Indels were identified and annotated between JD17 and them. Symbiotic nitrogen fixation (SNF) genes were identified and the effects from these variants were further evaluated. It was found that the coding sequences of 9 nitrogen fixation-related genes were greatly affected. The high-quality genome assembly of JD17 can serve as a valuable reference for soybean functional genomics research.

scholarly journals New records of ring nematodes, Bakernema enormese n. sp. and Criconema (Nothocriconemella) graminicola Loof, Wouts & Yeates, 1997 (Nematoda: Criconematidae) from natural forests of Vietnam

2019 ◽  
Vol 41 (3) ◽  
Author(s):  
Nguyen Ngoc Chau
Keyword(s):  
New Species ◽  
Body Size ◽  
New Records ◽  
Large Body ◽  
Lateral View ◽  
The Body ◽  
Natural Forests ◽  
Large Body Size ◽  
Stylet Length ◽  
North Vietnam

Bakernema enormese sp. n., collected from rhizosphere of forest wood trees in Muong Phang, Dien Bien Province (north Vietnam) is described and illustrated. The new species is characterized by large body size and stylet. In general, this new species is close to two existing species of the same genus, B. inaequale and B. dauniense by cuticle structure in transparent membranous projections which appear in lateral view as spine-like structures on each annulus. These structure arranged into several rows along the body. In morphology, the new species differs from B. inaequale and B. dauniense  by body and stylet length, i.e. 609–842 µm and 143.5–150 µm vs. 391–578 µm and 59–74 µm for B. inaequale and vs. 391–461 µm and 65–74 µm for B. dauniense. In addition, new species can be distinguished from B. inaequale by the longer membranous projection, 8–12 vs. 6–10 µm and vagina shape, curved vs. sigmoid. From B. dauniense, the new species differs by the much longer membranous projection, 8–12 vs. 1.4–2.2 µm and less number annules between vulva and tail end (RV), 3–4 vs. 7.8 annules. The presence of Criconema (Nothocriconemella) graminicola Loof, Wouts & Yeates, in Vietnam with morphometrics, illustrators and remarks given.

scholarly journals Genome-Wide Effects of Selenium and Translational Uncoupling on Transcription in the Termite Gut Symbiont Treponema primitia

mBio ◽  
2013 ◽  
Vol 4 (6) ◽  
Author(s):  
Eric G. Matson ◽  
Adam Z. Rosenthal ◽  
Xinning Zhang ◽  
Jared R. Leadbetter
Keyword(s):  
Protein Synthesis ◽  
Large Body ◽  
Transcriptional Responses ◽  
Translational Coupling ◽  
Genome Wide ◽  
A Genome ◽  
Protein Encoding ◽  
Termite Gut ◽  
Inhibiting Protein ◽  
Encoding Genes

ABSTRACTWhen prokaryotic cells acquire mutations, encounter translation-inhibiting substances, or experience adverse environmental conditions that limit their ability to synthesize proteins, transcription can become uncoupled from translation. Such uncoupling is known to suppress transcription of protein-encoding genes in bacteria. Here we show that the trace element selenium controls transcription of the gene for the selenocysteine-utilizing enzyme formate dehydrogenase (fdhFSec) through a translation-coupled mechanism in the termite gut symbiontTreponema primitia, a member of the bacterial phylumSpirochaetes. We also evaluated changes in genome-wide transcriptional patterns caused by selenium limitation and by generally uncoupling translation from transcription via antibiotic-mediated inhibition of protein synthesis. We observed that inhibiting protein synthesis inT. primitiainfluences transcriptional patterns in unexpected ways. In addition to suppressing transcription of certain genes, the expected consequence of inhibiting protein synthesis, we found numerous examples in which transcription of genes and operons is truncated far downstream from putative promoters, is unchanged, or is even stimulated overall. These results indicate that gene regulation in bacteria allows for specific post-initiation transcriptional responses during periods of limited protein synthesis, which may depend both on translational coupling and on unclassified intrinsic elements of protein-encoding genes.IMPORTANCEA large body of literature demonstrates that the coupling of transcription and translation is a general and essential method by which bacteria regulate gene expression levels. However, the potential role of noncanonical amino acids in regulating transcriptional output via translational control remains, for the most part, undefined. Furthermore, the genome-wide transcriptional state in response to translational decoupling is not well quantified. The results presented here suggest that the noncanonical amino acid selenocysteine is able to tune transcription of an important metabolic gene via translational coupling. Furthermore, a genome-wide analysis reveals that transcriptional decoupling produces a wide-ranging effect and that this effect is not uniform. These results exemplify how growth conditions that impact translational processivity can rapidly feed back on transcriptional productivity of prespecified groups of genes, providing bacteria with an efficient response to environmental changes.

scholarly journals Identification of loci affecting sexually dimorphic patterns for height and recurrent laryngeal neuropathy risk in American Belgian Draft Horses

2018 ◽  
Vol 50 (12) ◽  
pp. 1051-1058 ◽  
Author(s):  
Samantha A. Brooks ◽  
John Stick ◽  
Ashley Braman ◽  
Katelyn Palermo ◽  
N. Edward Robinson ◽  
...  
Keyword(s):  
Adult Height ◽  
Growth Traits ◽  
Treatment Strategies ◽  
Unknown Etiology ◽  
Specific Gene ◽  
Sexually Dimorphic ◽  
Haplotype Association ◽  
Genome Wide ◽  
A Genome ◽  
Specific Locus

Equine recurrent laryngeal neuropathy (RLN) is a bilateral mononeuropathy with an unknown etiology. In Thoroughbreds (TB), we previously demonstrated that the haplotype association for height (LCORL/NCAPG locus on ECA3, which affects body size) and RLN was coincident. In the present study, we performed a genome-wide association scan (GWAS) for RLN in 458 American Belgian Draft Horses, a breed fixed for the LCORL/NCAPG risk alelle. In this breed, RLN risk is associated with sexually dimorphic differences in height, and we identified a novel locus contributing to height in a sex-specific manner: MYPN (ECA1). Yet this specific locus contributes little to RLN risk, suggesting that other growth traits correlated to height may underlie the correlation to this disease. Controlling for height, we identified a locus on ECA15 contributing to RLN risk specifically in males. These results suggest that loci with sex-specific gene expression play an important role in altering growth traits impacting RLN etiology, but not necessarily adult height. These newly identified genes are promising targets for novel preventative and treatment strategies.

Sign in / Sign up

Export Citation Format

Share Document