Biology subjects

Zhou, B.

Publications and source records attributed to Zhou, B..

At least 199 records · Page 11Linked to original sources

bioRxiv2019

Microbial composition of the human nasopharynx varies according to influenza virus type and vaccination status.

Factors that contribute to enhanced susceptibility to severe bacterial disease after influenza infection are not well defined, but likely include the microbiome of the respiratory tract. Vaccination against influenza, while having variable effectiveness, could also play a role in microbial community stability. We collected nasopharyngeal samples from 215 individuals infected with influenza A/H3N2 or influenza B and profiled the microbiota by target sequencing of the 16S rRNA gene. We identified signature taxonomic groups by performing linear discriminant analysis and effective size comparisons (LEfSe) and defined bacterial community types using Dirichlet Multinomial Mixture (DMM) models. Influenza infection was shown to be significantly associated with microbial composition of the nasopharynx according to the virus type and the vaccination status of the patient. We identified 4 microbial community types across the combined cohort of influenza patients and healthy individuals with one community type most representative of the influenza-infected group. We also identified microbial taxa for which relative abundance was significantly higher in the unvaccinated elderly group; these taxa include species known to be associated with pneumonia.\n\nImportanceOur results suggest that there is a significant association between the composition of the microbiota in the nasopharynx and the influenza virus type causing the infection. We observe that vaccination status, especially in more senior individuals, also has an association with the microbial community profile. This indicates that vaccination against influenza, even when ineffective to prevent disease, could play a role in controlling secondary bacterial complications.

microbiology↗

bioRxiv2019

Predicting functional long non-coding RNAs validated by low throughput experiments

High-throughput techniques have uncovered hundreds and thousands of long non-coding RNAs (lncRNAs). Among them, only a small fraction has experimentally validated functions (EVlncRNAs) by low-throughput methods. What fraction of lncRNAs from high-throughput experiments (HTlncRNAs) is truly functional is an active subject of debate. Here, we developed the first method to distinguish EVlncRNAs from HTlncRNAs and mRNAs by using Support Vector Machines and found that EVlncRNAs can be well separated from HTlncRNAs and mRNAs with 0.6 for Matthews correlation coefficient, 64% for sensitivity, and 81% for precision for the independent human test set. The most discriminative features are related to sequence conservations at RNA (for separating from HTlncRNAs) and protein (for separating from mRNA) levels. The method is found to be robust as the human-RNA-trained model is applicable to independent mouse RNAs with similar accuracy and to a lesser extent to plant RNAs. The method can recover newly discovered EVlncRNAs with high sensitivity. Its application to randomly selected 2000 human HTlncRNAs indicates that a large number of functional lncRNAs are waiting to be validated. The method is expected to speed up and reduce the cost of the discovery by prioritizing potentially functional lncRNAs prior to experimental validation. EVlncRNA-pred is available as a web server at http://biophy.dzu.edu.cn/lncrnapred/index.html. All datasets used in this study can be obtained from the same website.

bioinformatics↗

bioRxiv2019

Low-background Acyl-biotinyl Exchange Largely Eliminates the Co-isolation of Non-S-acylated Proteins and Enables Deep S-acylproteomic Analysis

Protein S-acylation (also called palmitoylation) is a common post-translational modification whose deregulation plays a key role in the pathogenesis of many diseases. Acyl-biotinyl exchange (ABE), a widely used method for the enrichment of S-acylated proteins, has the potential of capturing the entire S-acylproteome in any types of biological samples. Here, we showed that current ABE methods suffer from high background arising from the co-isolation of non-S-acylated proteins. The background can be substantially reduced by an additional blockage of residual free cysteine residues with 2,2-dithiodipyridine prior to biotin-HPDP reaction. Coupling the low-background ABE (LB-ABE) method with label-free quantitative proteomics, 2,895 high-confidence candidate S-acylated proteins (including 1,591 known S-acylated proteins) were identified from human prostate cancer LNCaP cells, representing so-far the largest S-acylproteome dataset identified in a single study. Immunoblotting analysis confirmed the S-acylation of five known and five novel prostate cancer-related S-acylated proteins in LNCaP cells and suggested that their S-acylation levels were about 0.6-1.8%. In summary, the LB-ABE method largely eliminates the co-isolation of non-S-acylated proteins and enables deep S-acylproteomic analysis. It is expected to facilitate much more comprehensive and accurate quantification of S-acylproteomes than previous ABE methods.

biochemistry↗

bioRxiv2019

Vaccine blunts fentanyl potency in male rhesus monkeys

One proposed factor contributing to the increased opioid overdose deaths is the increased frequency of synthetic opioids, including fentanyl and fentanyl analogs. A treatment strategy currently under development to address the ongoing opioid crisis is immunopharmacotherapies or opioid-targeted vaccines. The present study determined the effectiveness and selectivity of a fentanyl-tetanus toxoid conjugate vaccine to alter the behavioral effects of fentanyl and a structurally dissimilar mu-opioid agonist oxycodone in male rhesus monkeys (n=3-4). Fentanyl and oxycodone produced dose-dependent suppression of behavior in an assay of schedule-controlled responding and antinociception in an assay of thermal nociception (50{degrees}C). Acute naltrexone (0.032 mg/kg) produced an approximate 10-fold potency shift for fentanyl to decrease operant responding. The fentanyl vaccine was administered at weeks 0, 2, 4, 9, 19, and 44 and fentanyl or oxycodone potencies in both behavioral assays were redetermined over the course of 49 weeks. The vaccine significantly and selectively shifted fentanyl potency at least 10-fold in both assays at several time points over the entire experimental period. Mid-point titer levels were significantly correlated with fentanyl antinociceptive potency shifts. Antibody affinity for fentanyl as measured by a competitive binding assay increased over time to around 3-4 nM. The fentanyl vaccine also significantly increased fentanyl plasma levels approximately 6-fold consistent with the hypothesis that the vaccine sequesters fentanyl in the blood. Overall, these results support the continued development and evaluation of this fentanyl vaccine to address the ongoing opioid crisis.\n\nHighlightsO_LIVaccine blunted fentanyl rate-suppression potency [~] 10-fold\nC_LIO_LIVaccine blunted fentanyl antinociceptive potency [~]25-fold\nC_LIO_LIFentanyl vaccine was as effective as acute 0.032 mg/kg naltrexone\nC_LIO_LIVaccine was selective for fentanyl and not oxycodone\nC_LIO_LIAntibody immune response [~] 3 nM affinity for fentanyl\nC_LI

neuroscience↗

bioRxiv2019

Comparative analysis of mitochondrial genome between UG93A and UG93B reveal common feature of 5’-end heterogeneity in mitochondrial genes of kenaf

Plant cytoplasmic male sterility (CMS) being maternal phenomenon trait that result from pollen abortion and closely linked with mitochondrial DNA rearrangement in many crops including kenaf. However, the molecular mechanism in kenaf is poorly known. In present work, we described the mitochondrial genome in isonuclear CMS line UG93A and its maintainer line UG93B. Findings of the current study revealed that a total of 398 SNPs and 230 InDels were identified in UG93A mtDNA. Total of 26 SNPs variations and three InDels were identified in the coding region of atp6, indicating its active role in mitochondrial genome re-arrangement. Northern blot analysis showed that the transcripts of atp1, atp4, atp6, cox3 and sdh4 in F1 were consistent with UG93A but different for UG93B. The transcript of atp9 was found similar between UG93B and F1 while different for UG93A, which depict that atp9 may be regulated by nuclear genes in F1 hybrid. The expression of atp9 in UG93A was substantially lower compared with UG93B, suggesting its key role for energy supplying in microspore development of kenaf. Circularized RNA (CR)-RT-PCR revealed that mitochondrial RNAs with heterogeneous 5-ends but uniform 3 - ends are common feature in kenaf mitochondrial genes, and the promoter architecture analysis showed that the promoter sequences in kenaf mitochondrial genome are highly diverged in comparison to those in other plants. Our data highlight that the translation of mitochondrial genes in kenaf is closely associated with heterogeneity of the 5-end of plant mRNA. The present result provides the basic information in understanding the transcription of kenaf mitochondrial genome and can be used as reference in other plants.

molecular biology↗

bioRxiv2018

Cell-to-cell variation in defective virus expression and effects on host responses during influenza virus infection

Virus and host factors contribute to cell-to-cell variation in viral infections and determine the outcome of the overall infection. However, the extent of the variability at the single cell level and how it impacts virus-host interactions at a systems level are not well understood. To characterize the dynamics of viral transcription and host responses, we used single-cell RNA sequencing to quantify at multiple time points the host and viral transcriptomes of human A549 cells and primary bronchial epithelial cells infected with influenza A virus. We observed substantial variability of viral transcription between cells, including the accumulation of defective viral genomes (DVGs) that impact viral replication. We show a correlation between DVGs and viral-induced variation of the host transcriptional program and an association between differential induction of innate immune response genes and attenuated viral transcription in subpopulations of cells. These observations at the single cell level improve our understanding of the complex virus-host interplay during influenza infection.\n\nIMPORTANCEDefective influenza virus particles generated during viral replication carry incomplete viral genomes and can interfere with the replication of competent viruses. These defective genomes are thought to modulate disease severity and pathogenicity of the influenza infection. Different defective viral genomes also introduce another source of variation across a heterogeneous cell population. Evaluating the impact of defective virus genomes on host cell responses cannot be fully resolved at the population level, requiring single cell transcriptional profiling. Here we characterized virus and host transcriptomes in individual influenza-infected cells, including that of defective viruses that arise during influenza A virus infection. We established an association between defective virus transcription and host responses and validated interfering and immunostimulatory functions of identified dominant defective virus genome species in vitro. This study demonstrates the intricate effects of defective viral genomes on host transcriptional responses and highlights the importance of capturing host-virus interactions at the single-cell level.

microbiology↗

bioRxiv2018

Astroglial dysfunctions drive aberrant synaptogenesis in developing brain with lengthy general anesthesia

Lengthy use of general anesthetics (GAs) causes cognitive deficits in developing brain, which has raised significant clinical concerns such that FDA is warning on the use of GAs in children younger than 3 years. However, the molecular and cellular mechanisms for GAs-induced neurotoxicity remain largely unknown. Here we report that sevoflurane, a commonly used GA in pediatrics, causes compromised astrocyte morphogenesis, spatiotemporally correlated to the synaptic overgrowth with reduced synaptic function in developing cortex in a regional-, exposure-length- and age-specific manner. Sevoflurane disrupts astrocyte Ca2+ homeostasis both acutely and chronically, which leads to the down regulation of Ezrin, an actin-binding membrane protein, which we found is critically involved in astrocyte morphogenesis in vivo. Importantly, in normal developing brain, the genetic intervention of astrocyte morphogenesis is sufficient to produce the aberrant synaptic structure and function virtually identical to the ones induced by lengthy sevoflurane exposure. Our data uncover that astrocytes are unexpectedly central targets for GAs to exert toxic effects, and that astrocyte morphological integrity is crucial for synaptogenesis in the developing brain.

neuroscience↗

bioRxiv2018

ApoE2, ApoE3 and ApoE4 Differentially Impact Multiple Signaling Pathways Regulating Synaptogenesis

Apolipoprotein E (ApoE) mediates clearance of circulating lipoproteins from blood by binding to ApoE receptors. Humans express three genetic variants, ApoE2, ApoE3, and ApoE4, that exhibit distinct ApoE receptor binding properties. In brain, ApoE is abundantly produced by activated astrocytes and microglia, and three variants differentially affect Alzheimers disease (AD), such that ApoE2 protects against, and ApoE4 predisposes to the disease. A role for ApoE4 in driving microglial dysregulation and impeding A{beta} clearance in AD is well documented, but the direct effects of three variants on neurons are poorly understood. Extending previous studies, we here demonstrate that ApoE variants differentially activate multiple neuronal signaling pathways and regulate synaptogenesis. Specifically, using human neurons cultured in the absence of glia to exclude indirect glial mechanisms, we show that ApoE broadly stimulates signal transduction cascades which among others enhance synapse formation with an ApoE4>ApoE3>ApoE2 potency rank order, paralleling the relative risk for AD conferred by these variants. Unlike the previously described induction of APP transcription, however, ApoE-induced synaptogenesis involves CREB rather than cFos activation. We thus propose that in brain, ApoE acts as a glia-secreted paracrine signal and activates neuronal signaling pathways in what may represent a protective response, with the differential potency of ApoE variants causing distinct levels of chronic signaling that may contribute to AD pathogenesis.

molecular biology↗

bioRxiv2018

Quantitative Proteomic Analysis of Prostate Tissue Specimens Identifies Deregulated ProteinComplexes in Primary Prostate Cancer

Prostate cancer (PCa) is the most frequently diagnosed non-skin cancer and a leading cause of mortality among males in developed countries. However, our understanding of the global changes of protein complexes within PCa tissue specimens remains very limited, although it has been well recognized that protein complexes carry out essentially all major processes in living organisms and that their deregulation drives the pathogenesis and progression of various diseases. By coupling tandem mass tagging-synchronous precursor selection-mass spectrometry/mass spectrometry/mass spectrometry (TMT-SPSMS3) with differential expression and co-regulation analyses, the present study compared the differences between protein complexes in normal prostate, low-grade PCa, and high-grade PCa tissue specimens. Globally, a large downregulated putative protein-protein interaction (PPI) network was detected in both low-grade and high-grade PCa, yet a large upregulated putative PPI network was only detected in high-grade but not low-grade PCa, compared with normal controls. To identify specific protein complexes that are deregulated in PCa, quantified proteins were mapped to protein complexes in CORUM, a collection of experimentally verified mammalian protein complexes. Differential expression analysis suggested that mitochondrial ribosomes and the fibrillin-associated protein complex were significantly overexpressed, whereas the ITGA6-ITGB4-Laminin10/12 and the P2X7 receptor signaling complexes were significantly downregulated, in PCa compared with normal prostate. Moreover, differential co-regulation analysis indicated that the assembly levels of some nuclear protein complexes involved in RNA synthesis and processing were significantly increased in low-grade PCa, and those of mitochondrial complex I and its subcomplexes were significantly increased in high-grade PCa, compared with normal prostate. In summary, the study represents the first global and quantitative comparison of protein complexes in prostate tissue specimens. It is expected to enhance our understanding of the molecular mechanisms underlying PCa development and progression in human patients, as well as lead to the discovery of novel biomarkers and therapeutic targets for precision management of PCa.

cancer biology↗

bioRxiv2018

A Genome-Wide Association Study Identifies SNP Markers for Virulence in Magnaporthe oryzae Isolates from Sub-Saharan Africa

The fungal phytopathogen Magnaporthe oryzae causes blast disease in cereals such as rice and finger millet worldwide. In this study, we assessed genetic diversity of 160 isolates from nine sub-Saharan Africa (SSA) and other principal rice producing countries and conducted a genome-wide association study (GWAS) to identify the genomic regions associated with virulence of M. oryzae. GBS of isolates provided a large and high-quality 617K single nucleotide polymorphism (SNP) dataset. Disease ratings for each isolate was obtained by inoculating them onto differential lines and locally-adapted rice cultivars. Genome-wide association studies were conducted using the GBS dataset and sixteen disease rating datasets. Principal Component Analysis (PCA) was used an alternative to population structure analysis for studying population stratification from genotypic data. A significant association between disease phenotype and 528 SNPs was observed in six GWA analyses. Homology of sequences encompassing the significant SNPs was determined to predict gene identities and functions. Seventeen genes recurred in six GWA analyses, suggesting a strong association with virulence. Here, the putative genes/genomic regions associated with the significant SNPs are presented.

genetics↗

bioRxiv2018

Allele-specific binding of RNA-binding proteins reveals functional genetic variants in the RNA

Allele-specific protein-RNA binding is an essential aspect that may reveal functional genetic variants influencing RNA processing and gene expression phenotypes. Recently, genome-wide detection of in vivo binding sites of RNA binding proteins (RBPs) is greatly facilitated by the enhanced UV crosslinking and immunoprecipitation (eCLIP) protocol. Hundreds of eCLIP-Seq data sets were generated from HepG2 and K562 cells during the ENCODE3 phase. These data afford a valuable opportunity to examine allele-specific binding (ASB) of RBPs. To this end, we developed a new computational algorithm, called BEAPR (Binding Estimation of Allele-specific Protein-RNA interaction). In identifying statistically significant ASB sites, BEAPR takes into account UV cross-linking induced sequence propensity and technical variations between replicated experiments. Using simulated data and actual eCLIP-Seq data, we show that BEAPR largely outperforms often-used methods Chi-Squared test and Fishers Exact test. Importantly, BEAPR overcomes the inherent over-dispersion problem of the other methods. Complemented by experimental validations, we demonstrate that ASB events are significantly associated with genetic regulation of splicing and mRNA abundance, supporting the usage of this method to pinpoint functional genetic variants in post-transcriptional gene regulation. Many variants with ASB patterns of RBPs were found as genetic variants with cancer or other disease relevance. About 38% of ASB variants were in linkage disequilibrium with single nucleotide polymorphisms from genome-wide association studies. Overall, our results suggest that BEAPR is an effective method to reveal ASB patterns in eCLIP and can inform functional interpretation of disease-related genetic variants.

bioinformatics↗

bioRxiv2018

Haplotype-phased Callithrix jacchus embryonic stem cell line for genome editing using CRISPR/Cas9

Due to anatomical and physiological similarities to humans, the common marmoset (Callithrix jacchus) is an ideal organism for the study human diseases. Researchers are currently leveraging genome-editing technologies such as CRISPR/Cas9 to genetically engineer marmosets for the in vivo biomedical modeling of human neuropsychiatric and neurodegenerative diseases. The genome characterization of these cell lines greatly reinforces these transgenic efforts. It also provides the genomic contexts required for the accurate interpretation of functional genomics data. We performed haplotype-resolved whole-genome characterization for marmoset ESC line cj367 from the Wisconsin National Primate Research Center. This is the first haplotype-resolved analysis of a marmoset genome and the first whole-genome characterization of any marmoset ESC line. We identified and phased single-nucleotide variants (SNVs) and Indels across the genome. By leveraging this haplotype information, we then compiled a list of cj367 ESC allele-specific CRISPR targeting sites. Furthermore, we demonstrated successful Cas9 Endonuclease Dead (dCas9) expression and targeted localization in cj367 as well as sustained pluripotency after dCas9 transfection by teratoma assay. Lastly, we show that these ESCs can be directly induced into functional neurons in a rapid, single-step process. Our study provides a valuable set of genomic resources for primate transgenics in this post-genome era.

genetics↗

bioRxiv2018

Haplotype-resolved and integrated genome analysis of ENCODE cell line HepG2

The HepG2 cancer cell line is one of the most widely-used biomedical research and one of the main cell lines of ENCODE. Vast numbers of functional genomics and epigenomics datasets have been produced to characterize its biology. However, the correct interpretation such data requires an understanding of the cell lines genome sequence and genome structure. Using a variety of sequencing and analysis methods, we identified a wide spectrum of HepG2 genome characteristics: copy numbers of chromosomal segments, SNVs and Indels (corrected for aneuploidy), phased haplotypes extending to entire chromosome arms, loss of heterozygosity, retrotransposon insertions, structural variants (SVs) including complex and somatic genomic rearrangements. We also identified allele-specific expression and DNA methylation genome-wide and assembled an allele-specific CRISPR/Cas9 targeting map.\n\nSIGNIFICANCEHaplotype-resolved and comprehensive whole-genome analysis of a widely-used cell line for cancer research and ENCODE, HepG2, serves as an essential resource for unlocking complex cancer gene regulation using a genome-integrated framework and also provides genomic context for the analysis of ~1,000 functional datasets to date on ENCODE for biological discovery. We also demonstrate how deeper insights into genomic regulatory complexity are gained by adopting a genome-integrated framework.

genomics↗

bioRxiv2018

Regulatory T-cells are required for neonatal heart regeneration

Previous work has elegantly demonstrated that, unlike adult mammalian heart, the neonatal heart is able to regenerate after injury from postnatal day (P) 1 to 7. Recently, macrophages are found to be required in the repair process as depletion of which abolishes endogenous regenerative capability of the neonatal heart. Nevertheless, whether innate immunity alone is sufficient for neonatal heart regeneration is obscure. Here, we investigate a hitherto novel role of FOXP3+ regulatory T-cells (Treg) in neonatal heart regeneration. Unlike their wild type counterparts, NOD/SCID mice that are deficient for T-cells but innate immune cells including macrophages fail to regenerate their injured heart as early as P3. In wild type mice, both conventional CD4+ T-cells and Treg are recruited to cardiac muscle within the first week after injury. Treatment with the lytic anti-CD4 antibody that specifically depletes conventional CD4+ T-cells leads to reduced cardiac fibrosis; while treatment with the lytic anti-CD25 antibody that specifically depletes CD4+CD25hiFOXP3+ Treg contributes to increased fibrosis of the neonatal heart after injury. Moreover, adoptive transfer of Treg to NOD/SCID mice results in mitigated fibrosis and increased proliferation and function of cardiac muscle of the neonatal heart after injury. Mechanistically, single cell transcriptomic profiling reveals that Treg are a source of chemokines and cytokines that attract monocytes and macrophages previously known to drive neonatal heart regeneration. Furthermore, Treg directly promote proliferation of both mouse and human cardiomyocytes in a paracrine manner. Our findings uncover an unappreciated mechanism in neonatal heart regeneration; and offer new avenues for developing novel therapeutics targeting Treg-mediated heart regeneration.

developmental biology↗

bioRxiv2018

Spatiotemporal Gene Coexpression and Regulation in Mouse Cardiomyocytes of Early Cardiac Morphogenesis

Cardiac looping is an early morphogenic process critical for the formation of four-chambered mammalian hearts. To study the roles of signaling pathways, transcription factors (TFs) and genetic networks in the process, we constructed gene co-expression networks and identified gene modules highly activated in individual cardiomyocytes (CMs) at multiple anatomical regions and developmental stages. Function analyses of the module genes uncovered major pathways important for spatiotemporal CM differentiation. Interestingly, about half of the pathways were highly active in cardiomyocytes at outflow tract (OFT) and atrioventricular canal (AVC), including many well-known signaling pathways for cardiac development and several newly identified ones. Most of the OFT-AVC pathways were predicted to be regulated by 6 6 transcription factors (TFs) actively expressed at the OFT-AVC locations, with the prediction supported by motif enrichment analysis of the TF targets, including 10 TFs that have not been previously associated with cardiac development, e.g., Etv5, Rbpms, and Baz2b. Finally, our study showed that the OFT-AVC TF targets were significantly enriched with genes associated with mouse heart developmental abnormalities and human congenital heart defects.

genetics↗

bioRxiv2018

Integrating Hi-C and FISH data for modeling 3D organizations of chromosomes

The new advances in various experimental techniques that provide complementary in-formation about the spatial conformations of chromosomes have inspired researchers to develop computational methods to fully exploit the merits of individual data sources and combine them to improve the modeling of chromosome structure. In this paper, we propose GEM-FISH, a first method for reconstructing the 3D models of chromosomes through systematically integrating both Hi-C and FISH data with the prior biophysical knowledge of a polymer model. Comprehensive tests on a set of chromosomes for which both Hi-C and FISH data were available have demonstrated that GEM-FISH can reconstruct the 3D models of chromosomes with more accurate spatial organizations of TADs and compartments than using only Hi-C data. In addition, GEM-FISH can accurately capture the spatial proximity of loop loci and the colocalization of loci from the same sub-compartments. Moreover, our reconstructed 3D models of chromosomes revealed novel patterns of spatial distributions of super-enhancers which can provide useful insights into understanding the functional roles of these super-enhancers in gene regulation. All these results demonstrated that, through integrating both Hi-C and FISH data into a unified framework, GEM-FISH can provide a better tool for modeling the 3D organizations of chromosomes than using the Hi-C data alone.

bioinformatics↗

bioRxiv2018

Sequencing of the Venter/HuRef genome using various strategies for the benchmarking of genome analysis tools

We produced an extensive collection of deep re-sequencing datasets for the Venter/HuRef genome using the Illumina massively-parallel DNA sequencing platform. The original Venter genome sequence is a very-high quality phased assembly based on Sanger sequencing. Therefore, researchers developing novel computational tools for the analysis of human genome sequence variation for the dominant Illumina sequencing technology can test and hone their algorithms by making variant calls from these Venter/HuRef datasets and then immediately confirm the detected variants in the Sanger assembly, freeing them of the need for further experimental validation. This process also applies to implementing and benchmarking existing genome analysis pipelines. We prepared and sequenced 200 bp and 350 bp short-insert whole-genome sequencing libraries (sequenced to 100x and 40x genomic coverages respectively) as well as 2 kb, 5 kb, and 12 kb mate-pair libraries (49x, 122x, and 145x physical coverages respectively). Lastly, we produced a linked-read library (128x physical coverage) from which we also performed haplotype phasing.

genomics↗

bioRxiv2017

The fruitENCODE project sheds light on the genetic and epigenetic basis of convergent evolution of climacteric fruit ripening

Fleshy fruit evolved independently multiple times during angiosperm history. Many climacteric fruits utilize the hormone ethylene to regulate ripening. The fruitENCODE project shows there are multiple evolutionary origins of the regulatory circuits that govern climacteric fruit ripening. Eudicot climacteric fruits with recent whole-genome duplications (WGDs) evolved their ripening regulatory systems using the duplicated floral identity genes, while others without WGD utilised carpel senescence genes. The monocot banana uses both leaf senescence and duplicated floral-identity genes, forming two interconnected regulatory circuits. H3K27me3 plays a conserved role in restricting the expression of key ripening regulators and their direct orthologs in both the ancestral dry fruit and non-climacteric fleshy fruit species. Our findings suggest that evolution of climacteric ripening was constrained by limited availability of signalling molecules and genetic and epigenetic materials, and WGD provided new resources for plants to circumvent this limit. Understanding these different ripening mechanisms makes it possible to design tailor-made ripening traits to improve quality, yield and minimize postharvest losses.\n\nOne Sentence SummaryThe fruitENCODE project discovered three evolutionary origins of the regulatory circuits that govern climacteric fruit ripening.

genomics↗