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 A genome-wide resource of cell cycle and cell shape genes of fission yeast

Open Biology ◽  
2013 ◽  
Vol 3 (5) ◽  
pp. 130053 ◽  
Author(s):  
Jacqueline Hayles ◽  
Valerie Wood ◽  
Linda Jeffery ◽  
Kwang-Lae Hoe ◽  
Dong-Uk Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Cell Shape ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Gene Deletions ◽  
Genome Wide ◽  
A Genome ◽  
Protein Encoding ◽  
Encoding Genes

To identify near complete sets of genes required for the cell cycle and cell shape, we have visually screened a genome-wide gene deletion library of 4843 fission yeast deletion mutants (95.7% of total protein encoding genes) for their effects on these processes. A total of 513 genes have been identified as being required for cell cycle progression, 276 of which have not been previously described as cell cycle genes. Deletions of a further 333 genes lead to specific alterations in cell shape and another 524 genes result in generally misshapen cells. Here, we provide the first eukaryotic resource of gene deletions, which describes a near genome-wide set of genes required for the cell cycle and cell shape.

scholarly journals Crosstalk in oxygen homeostasis networks: SKN-1/NRF inhibits the HIF-1 hypoxia-inducible factor in Caenorhabditis elegans

2021 ◽  
Author(s):  
Dingxia Feng ◽  
Zhiwei Zhai ◽  
Zhiyong Shao ◽  
Yi Zhang ◽  
Jo Anne Powell-Coffman
Keyword(s):  
Oxidative Stress ◽  
Hypoxia Inducible Factor ◽  
Regulatory Sequences ◽  
Low Oxygen ◽  
Transcriptional Responses ◽  
C Elegans ◽  
Protein Levels ◽  
Oxygen Homeostasis ◽  
Genome Wide ◽  
A Genome

AbstractDuring development, homeostasis, and disease, organisms must balance responses that allow adaptation to low oxygen (hypoxia) with those that protect cells from oxidative stress. The evolutionarily conserved hypoxia-inducible factors are central to these processes, as they orchestrate transcriptional responses to oxygen deprivation. Here, we employ genetic strategies in C. elegans to identify stress-responsive genes and pathways that modulate the HIF-1 hypoxia-inducible factor and facilitate oxygen homeostasis. Through a genome-wide RNAi screen, we show that RNAi-mediated mitochondrial or proteasomal dysfunction increases the expression of hypoxia-responsive reporter Pnhr-57:GFP in C. elegans. Interestingly, only a subset of these effects requires hif-1. Of particular importance, we found that skn-1 RNAi increases the expression of hypoxia-responsive reporter Pnhr-57:GFP and elevates HIF-1 protein levels. The SKN-1/NRF transcription factor has been shown to promote oxidative stress resistance. We present evidence that the crosstalk between HIF-1 and SKN-1 is mediated by EGL-9, the prolyl hydroxylase that targets HIF-1 for oxygen-dependent degradation. Treatment that induces SKN-1, such as heat, increases expression of a Pegl-9:GFP reporter, and this effect requires skn-1 function and a putative SKN-1 binding site in egl-9 regulatory sequences. Collectively, these data support a model in which SKN-1 promotes egl-9 transcription, thereby inhibiting HIF-1. We propose that this interaction enables animals to adapt quickly to changes in cellular oxygenation and to better survive accompanying oxidative stress.

Genome-wide characterization and analysis of F-box protein-encoding genes in the Malus domestica genome

2015 ◽  
Vol 290 (4) ◽  
pp. 1435-1446 ◽  
Author(s):  
Hao-Ran Cui ◽  
Zheng-Rong Zhang ◽  
Wei lv ◽  
Jia-Ning Xu ◽  
Xiao-Yun Wang
Keyword(s):  
Malus Domestica ◽  
Genome Wide ◽  
Protein Encoding ◽  
F Box Protein ◽  
Encoding Genes

scholarly journals HIV Genome-Wide Protein Associations: a Review of 30 Years of Research

2016 ◽  
Vol 80 (3) ◽  
pp. 679-731 ◽  
Author(s):  
Guangdi Li ◽  
Erik De Clercq
Keyword(s):  
Life Cycle ◽  
Viral Entry ◽  
Large Body ◽  
Viral Proteins ◽  
Host Cells ◽  
Comprehensive Overview ◽  
Genome Wide ◽  
A Genome ◽  
Glycoprotein Gp120 ◽  
Physical Interactions

SUMMARYThe HIV genome encodes a small number of viral proteins (i.e., 16), invariably establishing cooperative associations among HIV proteins and between HIV and host proteins, to invade host cells and hijack their internal machineries. As a known example, the HIV envelope glycoprotein GP120 is closely associated with GP41 for viral entry. From a genome-wide perspective, a hypothesis can be worked out to determine whether 16 HIV proteins could develop 120 possible pairwise associations either by physical interactions or by functional associations mediated via HIV or host molecules. Here, we present the first systematic review of experimental evidence on HIV genome-wide protein associations using a large body of publications accumulated over the past 3 decades. Of 120 possible pairwise associations between 16 HIV proteins, at least 34 physical interactions and 17 functional associations have been identified. To achieve efficient viral replication and infection, HIV protein associations play essential roles (e.g., cleavage, inhibition, and activation) during the HIV life cycle. In either a dispensable or an indispensable manner, each HIV protein collaborates with another viral protein to accomplish specific activities that precisely take place at the proper stages of the HIV life cycle. In addition, HIV genome-wide protein associations have an impact on anti-HIV inhibitors due to the extensive cross talk between drug-inhibited proteins and other HIV proteins. Overall, this study presents for the first time a comprehensive overview of HIV genome-wide protein associations, highlighting meticulous collaborations between all viral proteins during the HIV life cycle.

scholarly journals Pantoea agglomerans-Infecting Bacteriophage vB_PagS_AAS21: A Cold-Adapted Virus Representing a Novel Genus within the Family Siphoviridae

Viruses ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 479
Author(s):  
Monika Šimoliūnienė ◽  
Lidija Truncaitė ◽  
Emilija Petrauskaitė ◽  
Aurelija Zajančkauskaitė ◽  
Rolandas Meškys ◽  
...  
Keyword(s):  
Comparative Sequence Analysis ◽  
Pantoea Agglomerans ◽  
Open Reading Frames ◽  
Cold Adapted ◽  
Host Interactions ◽  
A Genome ◽  
Protein Encoding ◽  
The Family ◽  
Phage Propagation ◽  
Encoding Genes

A novel cold-adapted siphovirus, vB_PagS_AAS21 (AAS21), was isolated in Lithuania using Pantoea agglomerans as the host for phage propagation. AAS21 has an isometric head (~85 nm in diameter) and a non-contractile flexible tail (~174 × 10 nm). With a genome size of 116,649 bp, bacteriophage AAS21 is the largest Pantoea-infecting siphovirus sequenced to date. The genome of AAS21 has a G+C content of 39.0% and contains 213 putative protein-encoding genes and 29 genes for tRNAs. A comparative sequence analysis revealed that 89 AAS21 open reading frames (ORFs) code for unique proteins that have no reliable identity to database entries. In total, 63 AAS21 ORFs were functionally annotated, including those coding for the proteins responsible for virion morphogenesis, phage-host interactions, and DNA metabolism. Proteomic analysis led to the experimental identification of 19 virion proteins, including 11 that were predicted by bioinformatics approaches. Based on comparative phylogenetic analysis, AAS21 cannot be assigned to any genus currently recognized by ICTV and may represents a new branch of viruses within the family Siphoviridae.

scholarly journals A Genome-Wide View of Transcriptional Responses during Aphis glycines Infestation in Soybean

2020 ◽  
Vol 21 (15) ◽  
pp. 5191
Author(s):  
Luming Yao ◽  
Biyun Yang ◽  
Xiaohong Ma ◽  
Shuangshuang Wang ◽  
Zhe Guan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Expression Patterns ◽  
Aphis Glycines ◽  
Limiting Factors ◽  
Small Subset ◽  
Transcriptional Responses ◽  
Callose Deposition ◽  
Aphid Infestation ◽  
Genome Wide ◽  
A Genome

Soybean aphid (Aphis glycines Matsumura) is one of the major limiting factors in soybean production. The mechanism of aphid resistance in soybean remains enigmatic as little information is available about the different mechanisms of antibiosis and antixenosis. Here, we used genome-wide gene expression profiling of aphid susceptible, antibiotic, and antixenotic genotypes to investigate the underlying aphid–plant interaction mechanisms. The high expression correlation between infested and non-infested genotypes indicated that the response to aphid was controlled by a small subset of genes. Plant response to aphid infestation was faster in antibiotic genotype and the interaction in antixenotic genotype was moderation. The expression patterns of transcription factor genes in susceptible and antixenotic genotypes clustered together and were distant from those of antibiotic genotypes. Among them APETALA 2/ethylene response factors (AP2/ERF), v-myb avian myeloblastosis viral oncogene homolog (MYB), and the transcription factor contained conserved WRKYGQK domain (WRKY) were proposed to play dominant roles. The jasmonic acid-responsive pathway was dominant in aphid–soybean interaction, and salicylic acid pathway played an important role in antibiotic genotype. Callose deposition was more rapid and efficient in antibiotic genotype, while reactive oxygen species were not involved in the response to aphid attack in resistant genotypes. Our study helps to uncover important genes associated with aphid-attack response in soybean genotypes expressing antibiosis and antixenosis.

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 Genome-Wide Identification of NBS-Encoding Resistance Genes in Sunflower (Helianthus annuus L.)

Genes ◽  
2018 ◽  
Vol 9 (8) ◽  
pp. 384 ◽  
Author(s):  
Surendra Neupane ◽  
Ethan J. Andersen ◽  
Achal Neupane ◽  
Madhav P. Nepal
Keyword(s):  
Binding Site ◽  
Functional Divergence ◽  
Crop Improvement ◽  
Functional Characterization ◽  
Nucleotide Binding ◽  
Nucleotide Binding Site ◽  
Leucine Rich Repeat ◽  
Genome Wide ◽  
A Genome ◽  
Encoding Genes

Nucleotide Binding Site—Leucine-Rich Repeat (NBS-LRR) genes encode disease resistance proteins involved in plants’ defense against their pathogens. Although sunflower is affected by many diseases, only a few molecular details have been uncovered regarding pathogenesis and resistance mechanisms. Recent availability of sunflower whole genome sequences in publicly accessible databases allowed us to accomplish a genome-wide identification of Toll-interleukin-1 receptor-like Nucleotide-binding site Leucine-rich repeat (TNL), Coiled Coil (CC)-NBS-LRR (CNL), Resistance to powdery mildew 8 (RPW8)-NBS-LRR (RNL) and NBS-LRR (NL) protein encoding genes. Hidden Markov Model (HMM) profiling of 52,243 putative protein sequences from sunflower resulted in 352 NBS-encoding genes, among which 100 genes belong to CNL group including 64 genes with RX_CC like domain, 77 to TNL, 13 to RNL, and 162 belong to NL group. We also identified signal peptides and nuclear localization signals present in the identified genes and their homologs. We found that NBS genes were located on all chromosomes and formed 75 gene clusters, one-third of which were located on chromosome 13. Phylogenetic analyses between sunflower and Arabidopsis NBS genes revealed a clade-specific nesting pattern in CNLs, with RNLs nested in the CNL-A clade, and species-specific nesting pattern for TNLs. Surprisingly, we found a moderate bootstrap support (BS = 50%) for CNL-A clade being nested within TNL clade making both the CNL and TNL clades paraphyletic. Arabidopsis and sunflower showed 87 syntenic blocks with 1049 high synteny hits between chromosome 5 of Arabidopsis and chromosome 6 of sunflower. Expression data revealed functional divergence of the NBS genes with basal level tissue-specific expression. This study represents the first genome-wide identification of NBS genes in sunflower paving avenues for functional characterization and potential crop improvement.

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.

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