Biology subjects

Tang, Z.

Publications and source records attributed to Tang, Z..

At least 127 records · Page 7Linked to original sources

bioRxiv2021

Hydraulic diversity stabilizes productivity in a large-scale subtropical tree biodiversity experiment

Extreme climatic events threaten forests and their climate mitigation potential globally. Understanding the drivers promoting ecosystem stability is therefore considered crucial to mitigate adverse climate change effects on forests. Here, we use structural equation models to explain how tree species richness, asynchronous species dynamics and diversity in hydraulic traits affect the stability of forest productivity along an experimentally manipulated biodiversity gradient ranging from 1 to 24 tree species. Tree species richness improved stability by increasing species asynchrony. That is, at higher species richness, inter-annual variation in productivity among tree species buffered the community against stress-related productivity declines. This effect was mediated by the diversity of species hydraulic traits regarding drought tolerance and stomatal control, but not by the community-weighted means of these traits. The identified mechanisms by which tree species richness stabilizes forest productivity emphasize the importance of hydraulically diverse, mixed-species forests to adapt to climate change.

ecology↗

bioRxiv2020

Allantoin induces pruritus by activating MrgprD in chronic kidney disease

Chronic kidney disease is a disease with decreased, irreversible renal function. Pruritus is the most common skin symptom in patients with chronic kidney disease, especially in end-stage renal disease (AKA chronic kidney disease-associated pruritus [CKD-aP]); however, the underlying molecular and neural mechanism of the CKD-aP in patients remains obscure. Our data show that the level of allantoin increases in the serum of CKD-aP and CKD model mice. Allantoin could induce scratching behavior in mice and active DRG neurons; the calcium influx and the action potential were significantly reduced in DRG neurons of MrgprD KO or TRPV1 KO mice. U73122, an antagonist of PLC, could also block calcium influx in DRG neurons induced by allantoin. Thus, our results concluded that allantoin plays an important role in CKD-aP, mediated by MrgprD and TrpV1, in CKD patients.

pathology↗

bioRxiv2020

Co-infection of influenza A virus enhances SARS-CoV-2 infectivity

The upcoming flu season in the northern hemisphere merging with the current COVID-19 pandemic raises a potentially severe threat to public health. Through experimental co-infection of IAV with either pseudotyped or SARS-CoV-2 live virus, we found that IAV pre-infection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Remarkably, increased SARS-CoV-2 viral load and more severe lung damage were observed in mice co-infected with IAV in vivo. Moreover, such enhancement of SARS-CoV-2 infectivity was not seen with several other viruses probably due to a unique IAV segment as an inducer to elevate ACE2 expression. This study illustrates that IAV has a special nature to aggravate SARS-CoV-2 infection, and prevention of IAV is of great significance during the COVID-19 pandemic.

microbiology↗

bioRxiv2020

Wide-spectrum cancer killing by ENDOD1 ablation

The atypical nuclease ENDOD1 functions with cGAS-STING in innate immunity. Here we identify a previously uncharacterized ENDOD1 function in DNA repair. ENDOD1 is enriched in the nucleus following H2O2 treatment and ENDOD1-/- cells show increased PARP chromatin-association. Loss of ENDOD1 function is synthetic lethal with homologous recombination defects, with affected cells accumulating DNA double strand breaks. Remarkably, we also uncover an additional synthetic lethality between ENDOD1 and p53. ENDOD1 depletion in TP53 mutated tumour cells, or p53 depletion in ENDOD1-/- cells, results in rapid single stranded DNA accumulation and cell death. Because TP53 is mutated in [~]50% of tumours, ENDOD1 has potential as a wide-spectrum target for synthetic lethal treatments. To support this we demonstrate that systemic knockdown of mouse EndoD1 is well tolerated and whole-animal siRNA against human ENDOD1 restrains TP53 mutated tumour progression in xenograft models. These data identify ENDOD1 as a potential cancer-specific target for SL drug discovery.

cancer biology↗

bioRxiv2020

Disease Network Delineates the Disease Progression Profile of Cardiovascular Diseases

As Electronic Health Records (EHR) data accumulated explosively in recent years, the tremendous amount of patient clinical data provided opportunities to discover real world evidence. In this study, a graphical disease network, named progressive cardiovascular disease network (progCDN), was built based on EHR data from 14.3 million patients 1 to delineate the progression profiles of cardiovascular diseases (CVD). The network depicted the dominant diseases in CVD development, such as the heart failure and coronary arteriosclerosis. Novel progression relationships were also discovered, such as the progression path from long QT syndrome to major depression. In addition, three age-group progCDNs identified a series of age-associated disease progression paths and important successor diseases with age bias. Furthermore, we extracted a list of salient features to build a series of disease risk models based on the progression pairs in the disease network. The progCDN network can be further used to validate or explore novel disease relationships in real world data. Features with sufficient abundance and high correlation can be widely applied to train disease risk models when using EHR data.

bioinformatics↗

bioRxiv2020

rMVP: A Memory-efficient, Visualization-enhanced, and Parallel-accelerated tool for Genome-Wide Association Study

Along with the development of high-throughout sequencing technologies, both sample size and number of SNPs are increasing rapidly in Genome-Wide Association Studies (GWAS) and the associated computation is more challenging than ever. Here we present a Memory-efficient, Visualization-enhanced, and Parallel-accelerated R package called "rMVP" to address the need for improved GWAS computation. rMVP can: (1) effectively process large GWAS data; (2) rapidly evaluate population structure; (3) efficiently estimate variance components by EMMAX, FaST-LMM, and HE regression algorithms; (4) implement parallel-accelerated association tests of markers using GLM, MLM, and FarmCPU methods; (5) compute fast with a globally efficient design in the GWAS processes; and (6) generate various visualizations of GWAS related information. Accelerated by block matrix multiplication strategy and multiple threads, the association test methods embedded in rMVP are approximately 5-20 times faster than PLINK, GEMMA, and FarmCPU_pkg. rMVP is freely available at https://github.com/xiaolei-lab/rMVP.

genetics↗

bioRxiv2020

Piezo1 potentially mediates inflammation in balloon-inflated rat brain and its bidirectional mechanosensitivity

Brain injury after intracerebral hemorrhage is extremely complicated, and the exact mechanism remains puzzling. Piezo1, a novel mammalian mechanosensitive ion channel, has been identified to play important roles in several pathologic and physiologic procedures that involve cellular mechanotransduction. However, the role of Piezo1 in hematoma compression after intracerebral hemorrhage is still unclear. In the present study, we established a balloon-inflated rat brain model mimicking the pure mechanical compression of a hematoma and detected balloon compression in the basal ganglia region of the brain, resulting in abnormal behaviors and a significant increase in the expression of Piezo1 and proinflammatory cytokines. These effects were reversed by GsMTx4, an antagonist of Piezo1. Additionally, the balloon deflation time affected behavioral function and the levels of Piezo1 and proinflammatory cytokines. These results establish the first in vivo evidence for the role of Piezo1 in blood-brain neuroinflammation after hematoma compression. Piezo1 may therefore be a potential therapeutic target for the treatment of intracerebral hemorrhage.

neuroscience↗

bioRxiv2020

Drone phenotyping and machine learning enable discovery of loci regulating daily floral opening in lettuce

Flower opening and closure are traits of reproductive importance in all angiosperms because they determine the success of self- and cross-pollination. The temporal nature of this phenotype rendered it a difficult target for genetic studies. Cultivated and wild lettuce, Lactuca spp., have composite inflorescences comprised of multiple florets that open only once. Different accessions were observed to flower at different times of day. An F6 recombinant inbred line population (RIL) had been derived from accessions of L. serriola x L. sativa that originated from different environments and differed markedly for daily floral opening time. This population was used to map the genetic determinants of this trait; the floral opening time of 236 RILs was scored over a seven-hour period using time-course image series obtained by drone-based remote phenotyping on two occasions, one week apart. Floral pixels were identified from the images using a support vector machine (SVM) machine learning algorithm with an accuracy above 99%. A Bayesian inference method was developed to extract the peak floral opening time for individual genotypes from the time-stamped image data. Two independent QTLs, qDFO2.1 (Daily Floral Opening 2.1) and qDFO8.1, were discovered. Together, they explained more than 30% of the phenotypic variation in floral opening time. Candidate genes with non-synonymous polymorphisms in coding sequences were identified within the QTLs. This study demonstrates the power of combining remote imaging, machine learning, Bayesian statistics, and genome-wide marker data for studying the genetics of recalcitrant phenotypes such as floral opening time. One sentence summaryMachine learning and Bayesian analyses of drone-mediated remote phenotyping data revealed two genetic loci regulating differential daily flowering time in lettuce (Lactuca spp.).

genetics↗

bioRxiv2020

Impact of the radiated brain microenvironment on a panel of human patient-derived xenografts.

ObjectiveRadiotherapy, combined with surgical resection and chemotherapy, remains a first-line treatment for infiltrative gliomas. However, these tumor are not surgically curable, and often recur, even within the prior radiation field, and may demonstrate a more aggressive phenotype. We recently demonstrated that the radiated brain tumor microenvironment promotes tumor aggressiveness in an orthotopic patient-derived xenograft (PDX) model of glioblastoma (Mayo GBM 143). Importantly, high grade gliomas display diverse molecular phenotypes, and whether this genetic variability leads to divergent behaviour in the radiated tumor microenvironment is unknown. Herein, we characterize the effects of the irradiated brain microenvinroment on nine additional unique GBM cell lines to better understand the nuances of how tumor molecular phenotypes influence cellular dynamics. MethodsFemale athymic nude mice were randomly divided into cranial radiation (15 Gy) and non-radiated groups. Mice then underwent intracranial implantation with one of the selected PDX GBM cell lines (GBM 6, 10, 12, 39, 46, 76, 123, 164, 196; total n=8-15, per group, per line). GBM 6 cells were additionally implanted 6 months after completion of fractionated radiation (4Gy x 10 fractions or 2Gy x 30 fractions) vs sham radiation. Kaplan-Meyer (K-M) and log-rank tests were performed to compare the survival between irradiated and non-irradiated groups. ResultOf nine previously untested human GBM lines, we found that five demonstrated shorter survival in the pre-radiated brain (GBM 6, 46, 76, 164, 196); similar to previous observations with GBM 143. GBM 6 was also evaluated 6 months after fractionated radiation yielding similar results. However, two lines yielded prolonged survival in the pre-radiated brain (GBM 10, 12); GBM12 and 10 demonstrated the fastest baseline growth in the non-radiated brain; GBM 39, 123 whose rate of growth was not impacted by the radiated brain, demonstrated a an intermediate baseline growth rate between that of those positively and negatively impacted by the radiated brain microenvironment. No other clinical or molecular phenotype was found to consistently correlate with response to the radiated microenvironment. ConclusionAmong a total of 10 total human GBM lines evaluated to date, 60% induce faster mortality in a radiated microenvironment, and 20% induce slower mortality. These results highlight the likely critical impact of the irradiated microenvironment on tumor behaviour, yet illustrate that different tumors may exhibit opposing responses. Although further evaluation will be needed to understand mechanisms of divergent behavior, our data suggest the increased rate of growth in the radiated microenvironment may not apply to the fastest-growing tumor lines, which could instead demonstrate a paradoxical response.

cancer biology↗

bioRxiv2020

Combination of favorable gene haplotypes plays an important role in rice hybrid grain quality traits based on genome-wide association analysis

Yield level and grain quality determine the commercial potential of rice (Oryza sativa L.) varieties. Mining and using genes that control important rice grain quality characteristics are major tasks for plant breeders. Here, a genome-wide association study was conducted to determine the genetic bases of 12 rice grain quality traits in 113 varieties and 565 testcross hybrids. A total of 56 significant SNPs were associated with 9 of the traits in variety phenotypic, general combining ability, testcross hybrid phenotypic and mid-parental heterotic datasets, from which 45 novel loci were identified. The cumulative effects of superior alleles or favorable haplotypes of genes closest to significant quality trait-associated loci were found in the four datasets. Additionally, the favorable gene haplotypes performed better than those of superior alleles in the variety and testcross hybrid datasets. Pyramiding the favorable haplotypes of five cloned rice grain quality genes resulted in a very low amylose content and high yield in the latter. These testcross hybrids had rice grain qualities similar to their parental lines but with much higher yields. The amylose content, grain width and grain length predictions for potential hybrids among the 113 varieties using genomic selection based on the BayesB method revealed a performance trend similar to those the testcross hybrids in our study. Thus, the selection of combination of favorable rice quality-related gene haplotypes is recommended to breed hybrids with high yields and elite grain qualities.

genetics↗

bioRxiv2020

A small molecule that binds an RNA repeat expansion stimulates its decay via the exosome complex

We describe the design of a small molecule that binds the structure of a r(CUG) repeat expansion [r(CUG)exp] and reverses molecular defects in two diseases mediated by the RNA - myotonic dystrophy type 1 (DM1) and Fuchs endothelial corneal dystrophy (FECD). Thus, a single structure-specific ligand has potential therapeutic benefit for multiple diseases, in contrast to oligonucleotide-based modalities that are customized for each disease by nature of targeting the gene that harbors the repeat. Indeed, the small molecule binds the target with nanomolar affinity and >100-fold specificity vs. many other RNAs and DNA. Interestingly, the compounds downstream effects are different in the two diseases, owing to the location of the repeat expansion. In DM1, r(CUG)exp is harbored in the 3 untranslated region (UTR) of and mRNA, and the compound has no effect on the RNAs abundance. In FECD, however, r(CUG)exp is located in an intron, and the small molecule, by binding the repeat expansion, facilitates excision of the intron, which is then degraded by the exosome complex exonuclease, hRRP6. Thus, structure-specific, RNA-targeting small molecules can act disease-specifically to affect biology, either by disabling its gain-of-function mechanism (DM1) or by stimulating quality control pathways to rid a disease-affected cell of a toxic RNA (FECD). Significance statementMany different diseases are caused by toxic structured RNAs. Herein, we designed a lead small molecule that binds a toxic structure and rescues disease biology. We show that a structure-specific small molecule can improve disease-associated defects in two diseases that share the common toxic RNA structure. In one disease, the toxic structure is harbored in an intron and causes its retention. The compound facilitates processing of a retained intron, enabling the disease-affected cell to remove the toxic RNA.

cell biology↗

bioRxiv2020

LanD-like Flavoprotein-Catalyzed Aminovinyl-Cysteine Formation through Oxidative Decarboxylation and Cyclization of a Peptide at the C-Terminus

Aminovinyl-cysteine residues arise from processing the C-terminal O_SCPLOWLC_SCPLOW-Cys and an internal O_SCPLOWLC_SCPLOW-Ser/O_SCPLOWLC_SCPLOW-Thr or O_SCPLOWLC_SCPLOW-Cys of a peptide. Formation of these nonproteinogenic amino acids, which occur in a macrocyclic ring of diverse ribosomally synthesized lanthipeptides and non-lanthipeptides, remains poorly understood. Here, we report that LanD-like flavoproteins in the biosynthesis of distinct non-lanthipeptides share an unexpected dual activity for aminovinyl-cysteine formation. Each flavoprotein catalyzes oxidative decarboxylation of the C-terminal O_SCPLOWLC_SCPLOW-Cys and couples the resulting enethiol nucleophile with the internal residue to afford a thioether linkage for peptide cyclization. The cyclization step, which largely depends on proximity effect by positioning the enethiol intermediate with a bent conformation at the active site, can be substrate-dependent, proceeding inefficiently through nucleophilic substitution for an unmodified peptide or efficiently through Michael addition for a dehydrated/dethiolated peptide. Uncovering this unusual flavin-dependent paradigm for thioether residue formation advances the understanding in the biosynthesis of aminovinyl-cysteine-containing RiPPs and renews interest in flavoproteins, particularly those involved in non-redox transformations. LanD-like flavoproteins activity, which is flexible in peptide substrate and amenable for evolution by engineering, can be combined with different post-translational modifications for structural diversity, thereby holding promise for peptide macrocyclization/functionalization in drug development by chemoenzymatic or synthetic biology approaches.

biochemistry↗

bioRxiv2019

Longitudinal epi-transcriptome profiling reveals the crucial role of m6A in prenatal skeletal muscle development of pigs

BackgroundN6-methyladenosine (m6A) is the most abundant RNA modification and essentially participates in the regulation of skeletal muscle development. However, the status and function of m6A methylation in prenatal myogenesis remains unclear now. ResultsIn our present study, we first demonstrate that chemical suppression of m6A and knockdown METTL14 significantly inhibit the differentiation and promote the proliferation of C2C12 myoblast cells. The mRNA expression of m6A reader protein IGF2BP1, which functions to promote the stability of target mRNA, continually decreases during the prenatal skeletal muscle development. Thereafter, profiling transcriptome-wide m6A for six developmental stage of prenatal skeletal muscle, which spanning two important waves of pig myogenesis, were performed using a refined MeRIP sequencing technology that is optimal for small-amount of RNA samples. Highly dynamic m6A methylomes across different development stages were then revealed, with majority of the affected genes enriched in pathways of skeletal muscle development. In association with the transcriptome-wide alterations, transcriptional regulatory factors (MyoD) and differentiated markers (MyHC, MYH1) of muscle development are simultaneously regulated with m6A and IGF2BP1. Knockdown of IGF2BP1 also suppresses myotube formation and promotes cell proliferation. ConclusionsThe present study clarifies the dynamics of RNA m6A methylation in the regulation of prenatal skeletal muscle development, providing a data baseline for future developmental as well as biomedical studies of m6A functions in muscle development and disease.

genetics↗

bioRxiv2019

The adoptive transfer of BCG-induced T lymphocytes contributes to hippocampal cell proliferation and tempers anxiety-like behavior in immune deficient mice

1.We previously have reported that neonatal Bacillus Calmette-Guerin (BCG) vaccination improves neurogenesis and behavior in early life through affecting the neuroimmune milieu in the brain, but it is uncertain whether activation phenotypes and functional changes in T lymphocytes shape brain development. Here, we studied the effects of BCG vaccination via the adoptive transfer of T lymphocytes from the BALB/c wild-type mice into naive mice. Our results show that mice adoptive BCG-induced lymphocytes (BCG->naive mice) showed anxiolytic and antidepressant-like performance when completing an elevated plus maze (EPM) test. Meanwhile, BCG->naive mice possess more cell proliferation and newborn neurons than PBS->naive and nude mice in the hippocampus. IFN-{gamma} and IL-4 levels in the serum of BCG->naive mice also increased, while TNF- and IL-1{beta} levels were reduced relative to those of PBS->naive and nude mice. We further found that BCG->naive mice showed different repartition of CD4+ and CD8+ T cell to naive (CD62L+ CD44low), effector memory (CD62L- CD44hi), central memory (CD62L+ CD44hi) and acute/activated effector (CD62L- CD44low) cells in the spleen. Importantly, the adoptive transfer of BCG-induced T lymphocytes infiltrated into the dura mater and brain parenchyma of the nude mice. Activation phenotypes and functional changes in T lymphocytes are very likely to affect the neuroimmune milieu in the brain, and alterations in ratios of splenic CD4+ and CD8+ memory T cells may affect the expression of correlative cytokines in the serum, accounting for our behavioral results. We conclude thus that the adoptive transfer of BCG-induced T lymphocytes contributes to hippocampal cell proliferation and tempers anxiety-like behavior in immune deficient mice. Our work shows that BCG vaccination improves hippocampal cell proliferation outcomes and behaviors, likely as a result of splenic effector/memory T lymphocytes regulating the neuroimmune niche in the brain.

neuroscience↗

bioRxiv2019

Neurocomputational mechanisms underlying immoral decisions benefiting self or others

Immoral behavior often consists of weighing transgression of a moral norm against maximizing personal profits. One important question is to understand why immoral behaviors vary based on who receives specific benefits and what are the neurocomputational mechanisms underlying such moral flexibility. Here, we used model-based fMRI to investigate how immoral behaviors change when benefiting oneself or someone else. Participants were presented with offers requiring a tradeoff between a moral cost (i.e., profiting a morally bad cause) and a benefit for either oneself or a charity. Participants were more willing to obtain ill-gotten profits for themselves than for a charity, driven by a devaluation of the moral cost when deciding for their own interests. The subjective value of an immoral offer, computed as a linear summation of the weighed monetary gain and moral cost, recruited the ventromedial prefrontal cortex regardless of beneficiaries. Moreover, paralleling the behavioral findings, this region enhanced its functional coupling with mentalizing-related regions while deciding whether to gain morally-tainted profits for oneself vs. charity. Finally, individual differences in moral preference differentially modulated choice-specific signals in the dorsolateral prefrontal cortex according to who benefited from the decisions. These findings provide insights for understanding the neurobiological basis of moral flexibility.

neuroscience↗

bioRxiv2019

Dissemination of linezolid-resistance through sex pheromone plasmid transfer in Enterococcs faecalis

Despite recent recognition of the ATP-binding cassette protein OptrA as an important mediator of linezolid-resistance in Enterococcus faecalis worldwide, the mechanisms of optrA gene acquisition and transfer remain poorly understood. In this study, we performed comprehensive molecular and phenotypic profiling of 44 optrA-carrying E. faecalis clinical isolates with linezolid-resistance. Pulse-field gel electrophoresis and DNA hybridization revealed the presence of optrA in the plasmid in 26 (59%) isolates and in the chromosome in 18 (41%) isolates. Conjugation experiments showed a successful transfer of optrA in 88.5% (23/26) of isolates carrying optrA in plasmids while no transfer occurred in any isolates carrying optrA in the chromosome (0/18). All 23 transconjugants exhibited in vitro resistance to linezolid and several other antibiotics, and were confirmed to contain optrA and other resistance genes. Plasmid typing demonstrated a predominance (18/23 or 78%) of rep9-type plasmids (pCF10 prototype) known to be the best studied sex pheromone responsive plasmids. Full plasmid genome sequencing of one isolate revealed the presence of drug resistance genes (optrA and fexA) and multiple sex pheromone response genes in the same plasmid, which represents the first sex pheromone responsive plasmid carrying optrA from a clinical isolate. PCR-based genotyping revealed the presence of three key sex pheromone response genes (prgA, prgB and prgC) in almost all 23 optrA-carrying isolates tested. Finally, functional studies of these isolates by clumping induction assay detected different degrees of clumping in most of the 23 isolates. Our analysis strongly suggests that optrA-mediated linezolid-resistance can be widely disseminated through sex pheromone plasmid transfer.

microbiology↗

bioRxiv2019

Transcriptional reprogramming in fused cells is triggered by plasma-membrane diminution

Developing cells divide and differentiate, and in many tissues, such as bone, muscle, and placenta, cells fuse acquiring specialized functions. While it is known that fused-cells are differentiated, it is unclear what mechanisms trigger the programmatic-change, and whether cell-fusion alone drives differentiation. To address this, we employed a fusogen-mediated cell-fusion system involving undifferentiated cells in tissue culture. RNA-seq analysis revealed cell-fusion initiates a dramatic transcriptional change towards differentiation. Dissecting the mechanisms causing this reprogramming, we observed that after cell-fusion plasma-membrane surface area decreases through increased endocytosis. Consequently, glucose-transporters are internalized, and cytoplasmic-glucose and ATP transiently decrease. This low-energetic state activates AMPK, which inhibits YAP1, causing cell-cycle arrest. Impairing either endocytosis or AMPK prevents YAP1 inhibition and cell-cycle arrest after fusion. Together these data suggest that cell-fusion-induced differentiation does not need to rely on extrinsic-cues; rather the plasma-membrane diminishment forced by the geometric-transformations of cell-fusion cause transient cell-starvation that induces differentiation.

cell biology↗

bioRxiv2019

Chromosome-scale de novo assembly and phasing of a Chinese indigenous pig genome

Chinese indigenous pigs differ significantly from Western commercial pig breeds in phenotypic and genomic characteristics. Thus, building a high-quality reference genome for Chinese indigenous pigs is pivotal to exploring gene function, genome evolution and improving genetic breeding in pigs. Here, we report an ultrahigh-quality phased chromosome-scale genome assembly for a male Luchuan pig, a representative Chinese domestic breed, by generating and combining data from PacBio Sequel reads, Illumina paired-end reads, high-throughput chromatin conformation capture and BioNano optical map. The primary assembly is [~] 2.58 Gb in size with contig and scaffold N50s of 18.03 Mb and 140.09 Mb, respectively. Comparison between primary assembly and alternative haplotig reveals numerous haplotype-specific alleles, which provide a rich resource to study the allele-specific expression, epigenetic regulation, genome structure and evolution of pigs. Gene enrichment analysis indicates that the Luchuan-specific genes are predominantly enriched in Gene Ontology terms for phosphoprotein phosphatase activity, signaling receptor activity and phosphatidylinositol binding. We provide clear molecular evolutionary evidence that the divergence time between Luchuan and Duroc pigs is dated back to about 1.7 million years ago. Meanwhile, Luchuan exhibits fewer events of gene family expansion and stronger gene family contraction than Duroc. The positively selected genes (PSGs) in Luchuan pig significantly enrich for protein tyrosine kinase activity, microtubule motor activity, GTPase activator activity and ubiquitin-protein transferase activity, whereas the PSGs in Duroc pig enrich for G-protein coupled receptor activity. Overall, our findings not only provide key benchmark data for the pig genetics community, but also pave a new avenue for utilizing porcine biomedical models to study human health and diseases.

genomics↗