Exploring the apple genome reveals six ACC synthase genes expressed during fruit ripening

AbstractFruit ripening of apple is regulated by a plant hormone ethylene. Ethylene signaling is based on its biosynthesis in which ACC synthase (ACS) is the rate-limited enzyme and plays the most important role. By exploring the apple whole genome, we identified 19 ACS genes, and their expressions in fruit were investigated. Six ACS genes were expressed in fruit, including four new sequences. Out of these six genes, three were totally inhibited by 1-MCP (1-methylcyclopropene, an ethylene inhibitor), which were considered to work in System 2 ethylene; the others did not respond to 1-MCP, being considered to work in System 1 ethylene biosynthesis. This study showed that the whole genome can be used as a potential resource to identify new members of a multi-gene family important for a specific trait in apple

Comparison Between Flat and Round Peaches, Genomic Evidences of Heterozygosity Events

Bud sports occur in many plant species, including fruit trees. Although they are correlated with genetic variance in somatic cells, the mechanisms responsible for bud sports are mostly unknown. In this study, a peach bud sport whose fruit shape was transformed to round from flat was identified by next generation sequencing (NGS), and we provide evidence that a long loss of heterozygosity (LOH) event may be responsible for this alteration in fruit shape. Moreover, compared to the reference genome, we identified 237,476 high quality single nucleotide polymorphisms (SNPs) in the wild-type and bud sport genomes. Using this SNP set, a long LOH event was identified at the distal end of scaffold Pp06 of the bud sport genome. Haplotypes from 155 additional peach accessions were phased, suggesting that the homozygous distal end of scaffold Pp06 of the bud sport was likely derived from only one haplotype of the wild-type flat peach. A genome-wide association study (GWAS) of 127 peach accessions was conducted to associate a SNP found at 26,924,482 bp of scaffold Pp06 to differences in fruit shape. All accessions with round-shaped fruit were found to have an A/A genotype, while those with A/T, or T/T genotypes had flat-shaped fruits. Finally, we also found that 236 peach accessions and 141 Prunus species with round-type fruit were found to have an A/A genotype at this SNP, while 22 flat peach accessions had an A/T genotype. Taken together, our results suggest that genes flanking this A/T polymorphism, and haplotyped carrying the T allele may determine flat fruit shape in this population. Furthermore, the LOH event resulting in the loss of the haplotype carrying the T allele may therefore be responsible for fruit shape alteration in wild-type flat peach

Robust Multimodal Failure Detection for Microservice Systems

Proactive failure detection of instances is vitally essential to microservice systems because an instance failure can propagate to the whole system and degrade the system's performance. Over the years, many single-modal (i.e., metrics, logs, or traces) data-based nomaly detection methods have been proposed. However, they tend to miss a large number of failures and generate numerous false alarms because they ignore the correlation of multimodal data. In this work, we propose AnoFusion, an unsupervised failure detection approach, to proactively detect instance failures through multimodal data for microservice systems. It applies a Graph Transformer Network (GTN) to learn the correlation of the heterogeneous multimodal data and integrates a Graph Attention Network (GAT) with Gated Recurrent Unit (GRU) to address the challenges introduced by dynamically changing multimodal data. We evaluate the performance of AnoFusion through two datasets, demonstrating that it achieves the F1-score of 0.857 and 0.922, respectively, outperforming the state-of-the-art failure detection approaches

Retrospective seroepidemiology indicated that human enterovirus 71 and coxsackievirus A16 circulated wildly in central and southern China before large-scale outbreaks from 2008

<p>Abstract</p> <p>Background</p> <p>Large nationwide outbreaks of hand, foot, and mouth disease (HFMD) occurred in China from 2008; most of the cases were in children under 5 years. This study aims to identify the situation of natural human enterovirus 71 (HEV71) and coxsackievirus A16 (CVA16) infections in children before 2008 in China.</p> <p>Results</p> <p>Retrospective seroepidemiologic studies of HEV71 and CVA16 were performed with 900 serum samples collected from children ≤5 years of age in 2005. The samples were collected from 6 different geographical areas (Anhui, Guangdong, Hunan, Xinjiang, Yunnan, and Heilongjiang provinces) in mainland China. Of the 900 samples, 288 were positive for HEV71; the total positive rate was 32.0% and the geometric mean titer (GMT) was 1:8.5. Guangdong (43.7% and 1:10.8), Xinjiang (45.4% and 1:11.1), and Yunnan (43.4% and 1:12.0) provinces had relatively high rates of infection, while Heilongjiang province (8.1% and 1:4.9) had the lowest rate of infection. On the other hand, 390 samples were positive for CVA16; the total positive rate was 43.4% and the GMT was 1:9.5. Anhui (62.2% and 1:16.0) and Hunan (61.1% and 1:23.1) had relatively high rates, while Heilongjiang (8.0% and 1:4.6) had the lowest rate. Although there is a geographical difference in HEV71 and CVA16 infections, low neutralizing antibody positive rate and titer of both viruses were found in all 6 provinces.</p> <p>Conclusions</p> <p>This report confirmed that HEV71 and CVA16 had wildly circulated in a couple provinces in China before the large-scale outbreaks from 2008. This finding also suggests that public health measures to control the spread of HEV71 and CVA16 should be devised according to the different regional characteristics.</p

An emerging recombinant human enterovirus 71 responsible for the 2008 outbreak of Hand Foot and Mouth Disease in Fuyang city of China

Hand, foot and mouth disease (HFMD), a common contagious disease that usually affects children, is normally mild but can have life-threatening manifestations. It can be caused by enteroviruses, particularly Coxsackieviruses and human enterovirus 71 (HEV71) with highly variable clinical manifestations. In the spring of 2008, a large, unprecedented HFMD outbreak in Fuyang city of Anhui province in the central part of southeastern China resulted in a high aggregation of fatal cases. In this study, epidemiologic and clinical investigations, laboratory testing, and genetic analyses were performed to identify the causal pathogen of the outbreak. Of the 6,049 cases reported between 1 March and 9 May of 2008, 3023 (50%) were hospitalized, 353 (5.8%) were severe and 22 (0.36%) were fatal. HEV71 was confirmed as the etiological pathogen of the outbreak. Phylogenetic analyses of entire VP1 capsid protein sequence of 45 Fuyang HEV71 isolates showed that they belong to C4a cluster of the C4 subgenotype. In addition, genetic recombinations were found in the 3D region (RNA-dependent RNA polymerase, a major component of the viral replication complex of the genome) between the Fuyang HEV71 strain and Coxsackievirus A16 (CV-A16), resulting in a recombination virus. In conclusion, an emerging recombinant HEV71 was responsible for the HFMD outbreak in Fuyang City of China, 2008

Expression of CD82 in Human Trophoblast and Its Role in Trophoblast Invasion

BACKGROUND: Well-controlled trophoblast invasion at maternal-fetal interface is a critical event for the normal development of placenta. CD82 is a member of transmembrane 4 superfamily, which showed important role in inhibiting tumor cell invasion and migration. We surmised that CD82 are participates in trophoblast differentiation during placenta development. METHODOLOGY/PRINCIPAL FINDINGS: CD82 was found to be strongly expressed in human first trimester placental villous and extravillous trophoblast cells as well as in trophoblast cell lines. To investigate whether CD82 plays a role in trophoblast invasion and migration, we further utilized human villous explants culture model on matrigel and invasion/migration assay of trophoblast cell line HTR8/SVneo. CD82 siRNA significantly promoted outgrowth of villous explants in vitro (P<0.01), as well as invasion and migration of HTR8/SVneo cells (P<0.05), whereas the trophoblast proliferation was not affected. The enhanced effect of CD82 siRNA on invasion and migration of trophoblast cells was found associated with increased gelatinolytic activities of matrix metalloproteinase MMP9 while over-expression of CD82 markedly decreased trphoblast cell invasion and migration as well as MMP9 activities. CONCLUSIONS/SIGNIFICANCE: These findings suggest that CD82 is an important negative regulator at maternal-fetal interface during early pregnancy, inhibiting human trophoblast invasion and migration

Abnormalities in Osteoclastogenesis and Decreased Tumorigenesis in Mice Deficient for Ovarian Cancer G Protein-Coupled Receptor 1

Ovarian cancer G protein-coupled receptor 1 (OGR1) has been shown to be a proton sensing receptor in vitro. We have shown that OGR1 functions as a tumor metastasis suppressor gene when it is over-expressed in human prostate cancer cells in vivo. To examine the physiological functions of OGR1, we generated conditional OGR1 deficient mice by homologous recombination. OGR1 deficient mice were viable and upon gross-inspection appeared normal. Consistent with in vitro studies showing that OGR1 is involved in osteoclastogenesis, reduced osteoclasts were detected in OGR1 deficient mice. A pH-dependent osteoclasts survival effect was also observed. However, overall abnormality in the bones of these animals was not observed. In addition, melanoma cell tumorigenesis was significantly inhibited in OGR1 deficient mice. OGR1 deficient mice in the mixed background produced significantly less peritoneal macrophages when stimulated with thioglycolate. These macrophages also showed altered extracellular signal-regulated kinases (ERK) activation and nitric oxide (NO) production in response to lipopolysaccharide. OGR1-dependent pH responses assessed by cAMP production and cell survival in macrophages or brown fat cells were not observed, presumably due to the presence of other proton sensing receptors in these cells. Our results indicate that OGR1's role in osteoclastogenesis is not strong enough to affect overall bone development and its role in tumorigenesis warrants further investigation. The mice generated can be potentially used for several disease models, including cancers or osteoclast-related diseases

Systemic 7-methylxanthine in retarding axial eye growth and myopia progression: a 36-month pilot study

The adenosine antagonist 7-methylxanthine (7-mx) works against myopia in animal models. In a clinical trial, 68 myopic children (mean age 11.3 years) received either placebo or 7-mx tablets for 12 months. All participants subsequently received 7-mx for another 12 months, after which treatment was stopped. Axial length was measured with Zeiss IOL-Master and cycloplegic refraction with Nikon Retinomax at −6, 0, 12, 24, and 36 months. Axial growth was reduced among children treated with 7-mx for 24 months compared with those only treated for the last 12 months. Myopia progression and axial eye growth slowed down in periods with 7-mx treatment, but when the treatment was stopped, both myopia progression and axial eye growth continued with invariable speed. The results indicate that 7-mx reduces eye elongation and myopia progression in childhood myopia. The treatment is safe and without side effects and may be continued until 18–20 years of age when myopia progression normally stops