Biology subjects

Qu, Y.

Publications and source records attributed to Qu, Y..

138 records · Page 8Linked to original sources

bioRxiv2020

Brassinosteroids Suppress Ethylene Biosynthesis via Transcription Factor BZR1 in Pear and Apple Fruit

The plant hormone ethylene is important for the ripening of climacteric fruit, such as pear (Pyrus ussuriensis), and the brassinosteroid (BR) class of phytohormones affects ethylene biosynthesis during ripening, although via an unknown molecular mechanism. Here, we observed that exogenous BR treatment suppressed ethylene production during pear fruit ripening, and that the expression of the transcription factor PuBZR1 was enhanced by epibrassinolide (EBR) treatment during pear fruit ripening. PuBZR1 was shown to interact with PuACO1, which converts 1-aminocyclopropane-1-carboxylic acid (ACC) to ethylene, and suppress its activity. We also observed that BR-activated PuBZR1 bound to the promoters of PuACO1 and of PuACS1a, which encodes ACC synthase, and directly suppressed their transcription. Moreover, PuBZR1 suppressed the expression of transcription factor PuERF2 by binding its promoter, and PuERF2 bound to the promoters of PuACO1 and PuACS1a. We concluded that PuBZR1 indirectly suppresses the transcription of PuACO1 and PuACS1a through its regulation of PuERF2. Ethylene production and the expression profiles of the corresponding apple (Malus domestica) homologs showed similar changes following EBR treatment. Together, these results suggest that BR-activated BZR1 suppresses ACO1 activity and the expression of ACO1 and ACS1a, thereby reducing ethylene production during pear and apple fruit ripening. This likely represents a conserved mechanism by which exogenous BR suppresses ethylene biosynthesis during climacteric fruit ripening. One-sentence summaryBR-activated BZR1 suppresses ACO1 activity and expression of ACO1 and ACS1a, which encode two ethylene biosynthesis enzymes, thereby reducing ethylene production during pear and apple fruit ripening.

plant biology↗

bioRxiv2020

Transcriptomic and Proteomic Analyses of a New Cytoplasmic Male Sterile Line with wild Gossypium bickii. Genetic Background

Cotton is an important fiber crop but has serious effects of heterosis, in which cytoplasmic male sterility (CMS) being the major cause of heterosis in plants. However, there are no studies done on CMS Yamian A in cotton with the genetic background of the Australian wild Gossypium bickii. Transcriptomic and proteomic results showed that UDP-glucosyltransferase - in the nucleus, 60S ribosomal protein L13a- in the cytoplasm, ribulose-1,5-bisphosphate carboxylase/oxygenase - in the chloroplast, glutathione S-transferase - in the cytoplasm, and ATP synthase F1 subunit 1 - in the mitochondrion were upregulated; while low molecular weight heat shock protein - in the chloroplast and ATP synthase D chain- in the mitochondrion were down-regulated expression at the microspore abortion stage of Yamian A. We constructed an interaction network and this study provides a comprehensive understanding of the mechanism of CMS in cotton by use of in Yamian A, with wild cotton genetic background.

plant biology↗

bioRxiv2020

The Pathogenicity of 2019 Novel Coronavirus in hACE2 Transgenic Mice

Severe acute respiratory syndrome CoV-2 (SARS-CoV-2) caused the Corona Virus Disease 2019 (COVID-19) cases in China has become a public health emergency of international concern (PHEIC). Based on angiotensin converting enzyme 2 (ACE2) as cell entry receptor of SARS-CoV, we used the hACE2 transgenic mice infected with SARS-CoV-2 to study the pathogenicity of the virus. Weight loss and virus replication in lung were observed in hACE2 mice infected with SARS-CoV-2. The typical histopathology was interstitial pneumonia with infiltration of significant lymphocytes and monocytes in alveolar interstitium, and accumulation of macrophages in alveolar cavities. Viral antigens were observed in the bronchial epithelial cells, alveolar macrophages and alveolar epithelia. The phenomenon was not found in wild type mice with SARS-CoV-2 infection. The pathogenicity of SARS-CoV-2 in hACE2 mice was clarified and the Kochs postulates were fulfilled as well, and the mouse model may facilitate the development of therapeutics and vaccines against SARS-CoV-2.

microbiology↗

bioRxiv2020

A Grain of Salt

We quantified grain sodium (Na+) content across a barley GWAS panel grown under optimal conditions. We identified a strong association with a region containing two low and one high Na+ accumulating haplotypes of a Class 1 HIGH-AFFINITY POTASSIUM TRANSPORTER (HKT1;5) known to be involved in regulating plant Na+ homeostasis. The haplotypes exhibited an average 1.8-fold difference in grain Na+ content. We show that an L189P substitution disrupts Na+ transport in the high Na+ lines, disturbs the plasma membrane localisation typical of HKT1;5 and induces a conformational change in the protein predicted to compromise function. Under NaCl stress, lines containing P189 accumulate high levels of Na+, but show no significant difference in biomass. P189 increases in frequency from wild-species to elite cultivars leading us to speculate that the compromised haplotype is undergoing directional selection possibly due to the value of Na+ as a functional nutrient in non-saline environments.

genetics↗

bioRxiv2020

GmSALT3 confers shoot Na+ and Cl- exclusion in soybean via two distinct processes.

Soybean (Glycine max) yields are threatened by multiple stresses including soil salinity. GmSALT3 confers net shoot exclusion for both Na+ and Cl- and improves salt tolerance of soybean; however, how the ER-localised GmSALT3 achieves this is unknown. Here, GmSALT3s function was investigated in heterologous systems and near-isogenic lines that contained the full-length GmSALT3 (NIL-T; salt-tolerant) or a truncated transcript Gmsalt3 (NIL-S; salt-sensitive). GmSALT3 restored growth of K+-uptake-defective E. coli and contributed toward net influx and accumulation of Na+, K+, and Cl- in Xenopus laevis oocytes, while Gmsalt3 was non-functional. A time-course analysis of the NILs confirmed that shoot Cl- exclusion breaks down prior to Na+ exclusion, while grafting showed that shoot Na+ exclusion occurs via a root xylem-based mechanism. In contrast, NIL-T plants exhibited significantly greater Cl- content in both the stem xylem and phloem sap compared to NIL-S, indicating that shoot Cl- exclusion likely depends upon novel phloem-based Cl- recirculation. NIL-T shoots grafted on NIL-S roots contained low shoot Cl-, which confirmed that Cl- recirculation is dependent on the presence of GmSALT3 in shoots. Overall, these findings provide new insights on GmSALT3s impact on salinity tolerance and reveal a novel mechanism for shoot Cl- exclusion in plants. HighlightGmSALT3 improves soybean salt tolerance. Here, using heterologous expression, we found GmSALT3 is a functional ion transporter, and, in planta that it confers shoot salt exclusion through root-based Na+ xylem exclusion and shoot-based Cl- exclusion via phloem derived Cl- recirculation.

plant biology↗

bioRxiv2020

Endomembrane Cation Chloride Cotransporters (CCC1s) modulate endo- and exocytosis

Plant cells maintain a low luminal pH in the Trans-Golgi-Network/Early Endosome (TGN/EE), the organelle in which the secretory and endocytic pathways intersect. Impaired TGN/EE pH regulation translates into severe plant growth defects. The identity of the proton pump and proton/ion antiporters that regulate TGN/EE pH have been determined, but an essential component required to complete the TGN/EE membrane transport circuit remains unidentified - a pathway for cation and anion efflux. Here, we have used complementation, genetically encoded fluorescent sensors, and pharmacological treatments to demonstrate that the TGN/EE localised Arabidopsis Cation Chloride Cotransporter (CCC1) is this missing component necessary for regulating TGN/EE pH and function. Loss of CCC1 function leads to alterations in TGN/EE-mediated processes including endo- and exocytosis, and trafficking to the vacuole, and response to abiotic stress, consistent with the multitude of phenotypes observed in ccc1 knockout plants. This discovery places CCC1 as a central component of plant cellular function.

plant biology↗

bioRxiv2019

Extensive genetic diversity of bat-borne polyomaviruses reveals inter-family host-switching events

Polyomaviruses (PyVs) are small, double-stranded DNA tumor viruses carried by diverse vertebrates. PyVs have previously been considered highly host restricted in mammalian hosts, with host-switching events thought rare or nonexistent. Prior investigations have revealed short-range host-switching events of PyVs in two different African bat species within the horseshoe bat genus Rhinolophus. Herein, we have conducted a systematic investigation of PyVs in 1,083 archived bat samples collected from five provinces across China, and identified 192 PyVs from 186 bats from 15 host species within 6 families (Rhinolophidae, Vespertilionidae, Hipposideridae, Emballonuridae, Miniopteridae and Pteropodidae) representing 28 newly-described PyVs, indicative of extensive genetic diversity of bat PyVs. Surprisingly, two PyVs were identified in multiple bat species from different families, and another PyV clustered phylogenetically with PyVs carried by bats from a different host family, indicative of three inter-family PyV host-switching events. The time to most recent common ancestor (tMRCA) of the three events was estimated at 0.02-11.6 million years ago (MYA), which is inconsistent with the estimated tMRCA of their respective bat hosts (36.3-66.7 MYA), and is most parsimoniously explained by host-switching events. PyVs identified from geographically separated Chinese horseshoe bat species in the present study showed close genetic identities, and clustered with each other and with PyVs from African horseshoe bats, allowing assessment of the effects of positive selection in VP1 within the horseshoe bat family Rhinolophidae. Correlation analysis indicated that co-evolution with their hosts contributed much more to evolutionary divergence of PyV than geographic distance. In conclusion, our findings provide the first evidence of inter-family host-switching events of PyV in mammals and challenge the prevailing evolutionary paradigm for strict host restriction of mammalian PyVs.\n\nAuthor summarySince the discovery of murine polyomavirus in the 1950s, polyomaviruses (PyVs) have been considered both genetically stable and highly host-restricted in their mammalian hosts. In this study, we have identified multiple cases of host-switching events of PyVs by large scale surveillance in diverse bat species collected in China. These host-switching events occurred between bat families living in the same colony, indicating that a large population with frequent contacts between different bat species may represent an ecological niche facilitating PyV host-switching. The cases studied involved members of bats from several families, including horseshoe bats, which were previously found to harbor a number of highly virulent viruses to both humans and domestic animals. Our findings have provided evidence that even highly host-specific DNA viruses can transmit between bats of different species and indicate an increased propensity for spillover events involving horseshoe bats. We propose an evolutionary scheme for bat-borne PyVs in which intra-host divergence and host-switching has generated the diverse PyVs in present day bats. This scheme provides a useful model to study the evolution of PyVs in other hosts and, potentially, the modeling of bat zoonoses and the transmission of other DNA viruses in other mammals, including humans.

microbiology↗

bioRxiv2019

Cell cycle inhibitor Whi5 records environmental information to coordinate growth and division in yeast

Proliferating cells need to evaluate the environment to determine the optimal timing for cell cycle entry, which is essential for coordinating cell division and growth. In the budding yeast Saccharomyces cerevisiae, the commitment to the next round of division is made in G1 at the Start, triggered by the inactivation of the inhibitor Whi5 through multiple mechanisms. However, how a cell reads environmental condition and uses this information to regulate Start is poorly understood. Here, we show that Whi5 is a key environmental indicator and plays a crucial role in coordinating cell growth and division. We found that under a variety of nutrient and stress conditions, the concentration of Whi5 in G1 is proportional to the doubling time in the environment. Thus, under a poorer condition a longer doubling time results in a higher Whi5 concentration, which in turn delays the next cell cycle entry to ensure sufficient cell growth. In addition, the coordination between division and the environment is further fine-tuned in G1 by environmentally dependent G1 cyclin-Cdk1 contribution and Whi5 threshold at Start. Our results show that Whi5 serves as an environmental memory and that the cell adopts a simple and elegant mechanism to achieve an adaptive cellular decision making.

systems biology↗

bioRxiv2018

Efa6 regulates axon growth, branching and maintenance by eliminating off-track microtubules at the cortex

Cortical collapse factors affect microtubule (MT) dynamics at the plasma membrane. They play important roles in neurons, as suggested by inhibition of axon growth and regeneration through the Arf activator Efa6 in C. elegans, and by neurodevelopmental disorders linked to the mammalian kinesin Kif21A. How cortical collapse factors influence axon growth is little understood. Here we studied them, focussing on the function of Drosophila Efa6 in experimentally and genetically amenable fly neurons. First, we show that Drosophila Efa6 can inhibit MTs directly without interacting molecules via an N-terminal 18 amino acid motif (MT elimination domain/MTED) that binds tubulin and inhibits microtubule growth in vitro and cells. If N-terminal MTED-containing fragments are in the cytoplasm they abolish entire microtubule networks of mouse fibroblasts and whole axons of fly neurons. Full-length Efa6 is membrane-attached, hence primarily blocks MTs in the periphery of fibroblasts, and explorative MTs that have left axonal bundles in neurons. Accordingly, loss of Efa6 causes an increase of explorative MTs: in growth cones, they enhance axon growth, in axon shafts, explorative MTs cause excessive branching, as well as atrophy through perturbations of MT bundles. Efa6 over-expression causes the opposite phenotypes. Taken together, our work conceptually links molecular and sub-cellular functions of cortical collapse factors to axon growth regulation and reveals new roles in axon branching and in the prevention of axonal atrophy. Furthermore, the MTED delivers a promising tool that can be used to inhibit MTs in a compartmentalised fashion when fusing it to specifically localising protein domains.\n\nSummary statementThe cortical collapse factor Efa6 inhibits microtubule polymerising outside axonal bundles. Thereby it limits axon growth and branching, but preserves microtubule bundle organisation crucial for axon maintenance.

cell biology↗

bioRxiv2018

Genetic Dissection of Haploid Male Fertility in Maize (Zea mays L.)

Haploid genome doubling is a key limiting step of haploid breeding in maize. Spontaneous restoration of haploid male fertility (HMF) provides a method by which costs can be saved and which does not require the use of toxic chemicals, in contrast to the artificial doubling process. To reveal the genetic basis of HMF, haploids were obtained from the offspring of 285 F2:3 families, derived from the cross Zheng58x K22. The F2:3 families were used as female donor and YHI-1 as the male inducer line. The rates of HMF from each family line were evaluated at two field sites over two planting seasons. Quantitative trait loci (QTL) for HMF were identified using a genetic linkage map containing 157 simple sequence repeat (SSR) markers. QTL for HMF displayed incomplete dominance. Transgressive segregation of haploids from F2:3 families was observed relative to haploids derived from the two parents of the mapping population. A total of nine QTL were detected, which were distributed on chromosomes 1, 3, 4, 7, and 8. Three QTL, qHMF3b, qHMF7a, and qHMF7b were detected in both locations, respectively. In our mapping population, HMF was controlled by three major QTL. These QTL could be useful to predict the ability of spontaneous haploid genome doubling in related breeding materials, and to accelerate the haploid breeding process by introgression or aggregation of those QTL.

genetics↗

bioRxiv2017

Exchange protein directly activated by cAMP plays a critical role in regulation of vascular fibrinolysis

RationaleTo maintain vascular patency, endothelial cells (ECs) actively regulate hemostasis. Among the myriad of pathways by which they control both fibrin formation and fibrinolysis is EC expression of annexin A2 (ANXA2) in a heterotetrameric complex with S100A10 [(ANXA2-S100A10)2]. This complex is a well-recognized endothelial surface platform for the activation of plasminogen by tissue plasminogen activator. A noteworthy advance in this field came about when it was shown that the cAMP pathway is linked to the regulation of (ANXA2-S100A10)2 in ECs.\n\nObjectiveThese findings prompted us to determine whether a druggable target, namely the exchange protein directly activated by cAMP (EPAC) pathway, plays a role in vascular luminal fibrinolysis.\n\nMethods and ResultsTaking advantage of our Epac1-null mouse model, we found that depletion of Epac1 results in fibrin deposition, fibrinolytic dysfunction, and decreased endothelial surface ANXA2 in mice, which are similar to phenomena discovered in ANXA2-null and S100A10-null mice. We observed upregulation of EPAC1 and downregulation of fibrin in endocardial tissues beneath atrial mural thrombi in humans. Of note, our thrombosis model revealed that dysfunction of fibrinolysis in EPAC1-null mice can be ameliorated by recombinant ANXA2. Furthermore, we demonstrated that suppression of EPAC1 using a small-molecule inhibitor (ESI09) reduces the expression of ANXA2 in lipid rafts and impedes ANXA2 association with S100A10. Endothelial apical surface expression of both ANXA2 and S100A10 were markedly decreased in ESI09-treated ECs, which was corroborated by results from a nanoforce spectroscopy study. Moreover, inactivation of EPAC1 decreases tyrosine 23 phosphorylation of ANXA2 in the cell membrane compartment.\n\nConclusionsOur data reveal a novel role for EPAC1 in vascular fibrinolysis, by showing that EPAC1 is responsible for the translocation of ANXA2 to the EC surface. This process promotes conversion of plasminogen to plasmin, thereby enhancing local fibrinolytic activity.

cell biology↗

bioRxiv2017

Drosophila Short stop as a paradigm for the role and regulation of spectraplakins

Spectraplakins are evolutionarily well conserved cytoskeletal linker molecules that are true members of three protein families: plakins, spectrins and Gas2-like proteins. Spectraplakin genes encode at least 7 characteristic functional domains which are combined in a modular fashion into multiple isoforms, and which are responsible for an enormous breadth of cellular functions. These functions are related to the regulation of actin, microtubules, intermediate filaments, intracellular organelles, cell adhesions and signalling processes during the development and maintenance of a wide variety of tissues. To gain a deeper understanding of this enormous functional diversity, invertebrate genetic model organisms, such as the fruit fly Drosophila, can be used to develop concepts and mechanistic paradigms that can inform the investigation in higher animals or humans. Here we provide a comprehensive overview of our current knowledge of the Drosophila spectraplakin Short stop (Shot). We describe its functional domains and isoforms and compare them with those of the mammalian spectraplakins dystonin and MACF1. We then summarise its roles during the development and maintenance of the nervous system, epithelia, oocytes and muscles, taking care to compare and contrast mechanistic insights across these functions in the fly, but especially also with related functions of dystonin and MACF1 in mostly mammalian contexts. We hope that this review will improve the wider appreciation of how work on Drosophila Shot can be used as an efficient strategy to promote the fundamental concepts and mechanisms that underpin spectraplakin functions, with important implications for biomedical research into human disease.

cell biology↗