scholarly journals Transcription factor WRKY22 regulates canker susceptibility in sweet orange (Citrus sinensis Osbeck) by enhancing cell enlargement and CsLOB1 expression

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Qin Long ◽  
Meixia Du ◽  
Junhong Long ◽  
Yu Xie ◽  
Jingyun Zhang ◽  
...  
Keyword(s):  
Citrus Sinensis ◽  
Sweet Orange ◽  
Citrus Canker ◽  
Cell Enlargement ◽  
Transcription Start ◽  
Spongy Mesophyll ◽  
Pathological Hypertrophy ◽  
Cell Wall Organization

AbstractPathological hypertrophy (cell enlargement) plays an important role in the development of citrus canker, but its regulators are largely unknown. Although WRKY22 is known to be involved in pathogen-triggered immunity and positively regulates resistance to bacterial pathogens in Arabidopsis, rice and pepper, the CRISPR/Cas9-mediated partial knockout of CsWRKY22 improves resistance to Xanthomonas citri subsp. citri (Xcc) in Wanjincheng orange (Citrus sinensis Osbeck). Here, we demonstrate that CsWRKY22 is a nucleus-localized transcriptional activator. CsWRKY22-overexpressing plants exhibited dwarf phenotypes that had wrinkled and thickened leaves and were more sensitive to Xcc, whereas CsWRKY22-silenced plants showed no visible phenotype changes and were more resistant to Xcc. Microscopic observations revealed that the overexpression of CsWRKY22 increased cell size in the spongy mesophyll. Transcriptome analysis showed that cell growth-related pathways, such as the auxin and brassinosteroid hormonal signaling and cell wall organization and biogenesis pathways, were significantly upregulated upon CsWRKY22 overexpression. Interestingly, CsWRKY22 activated the expression of CsLOB1, which is a key gene regulating susceptibility to citrus canker. We further confirmed that CsWRKY22 bound directly to the W-boxes just upstream of the transcription start site of CsLOB1 in vivo and in vitro. We conclude that CsWRKY22 enhances susceptibility to citrus canker by promoting host hypertrophy and CsLOB1 expression. Thus, our study provides new insights into the mechanism regulating pathological hypertrophy and the function of WRKY22 in citrus.

scholarly journals New Promising Citrus Triploid Hybrids Selected from Crosses between Monoembryonic Diploid Female and Tetraploid Male Parents

HortScience ◽  
2005 ◽  
Vol 40 (3) ◽  
pp. 516-520 ◽  
Author(s):  
G. Reforgiato Recupero ◽  
G. Russo ◽  
S. Recupero
Keyword(s):  
Chromosome Number ◽  
Citrus Sinensis ◽  
Sweet Orange ◽  
Female Parent ◽  
In Vitro Cultivation ◽  
Diploid Female ◽  
Somatic Tissues ◽  
Fortunella Hindsii

The breeding of citrus triploid hybrids started at Istituto Sperimentale per l'Agrumicoltura spell out in Acireale, Italy, in 1978 (Starrantino and Reforgiato, 1981). The strategy used has been to cross a monoembryonic 2x female parent with a 4x male parent. The imbalance between the embryo and endosperm ploidy (3:4) makes seeds from such crossings incapable of germinating in vivo. However, in vitro cultivation has been used to rescue the embryos. In this paper we report the main characteristics of triploid hybrids from 22 different parents, including sweet orange [Citrus sinensis (L.) Osbeck], mandarin (C. reticulata Blanco), clementine (C. reticulata Blanco), grapefruit (C. paradisi Macf.), pummelo [C.maxima], tangor (C. reticulata × C. sinensis), lemon [C. limon (L.) Burm. f.], citron (C. medica L.), and Fortunella hindsii (Champ.) Swing. Tetraploid parents are duplex because they originate from the doubling of chromosome number of the nucella or of other somatic tissues. The segregation and recombination process results in triploid hybrids with characteristics that are nearer to the 4x parent than the 2x one. This strategy is important in obtaining seedless hybrids similar to a parent after generations of backcrossing.

scholarly journals Interactions between RNA polymerase and the core recognition element are a determinant of transcription start site selection

2016 ◽  
Vol 113 (21) ◽  
pp. E2899-E2905 ◽  
Author(s):  
Irina O. Vvedenskaya ◽  
Hanif Vahedian-Movahed ◽  
Yuanchao Zhang ◽  
Deanne M. Taylor ◽  
Richard H. Ebright ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Transcription Start Site ◽  
Transcription Initiation ◽  
Specific Protein ◽  
Start Site ◽  
Transcription Start ◽  
Transcription Bubble ◽  
Recognition Element

During transcription initiation, RNA polymerase (RNAP) holoenzyme unwinds ∼13 bp of promoter DNA, forming an RNAP-promoter open complex (RPo) containing a single-stranded transcription bubble, and selects a template-strand nucleotide to serve as the transcription start site (TSS). In RPo, RNAP core enzyme makes sequence-specific protein–DNA interactions with the downstream part of the nontemplate strand of the transcription bubble (“core recognition element,” CRE). Here, we investigated whether sequence-specific RNAP–CRE interactions affect TSS selection. To do this, we used two next-generation sequencing-based approaches to compare the TSS profile of WT RNAP to that of an RNAP derivative defective in sequence-specific RNAP–CRE interactions. First, using massively systematic transcript end readout, MASTER, we assessed effects of RNAP–CRE interactions on TSS selection in vitro and in vivo for a library of 47 (∼16,000) consensus promoters containing different TSS region sequences, and we observed that the TSS profile of the RNAP derivative defective in RNAP–CRE interactions differed from that of WT RNAP, in a manner that correlated with the presence of consensus CRE sequences in the TSS region. Second, using 5′ merodiploid native-elongating-transcript sequencing, 5′ mNET-seq, we assessed effects of RNAP–CRE interactions at natural promoters in Escherichia coli, and we identified 39 promoters at which RNAP–CRE interactions determine TSS selection. Our findings establish RNAP–CRE interactions are a functional determinant of TSS selection. We propose that RNAP–CRE interactions modulate the position of the downstream end of the transcription bubble in RPo, and thereby modulate TSS selection, which involves transcription bubble expansion or transcription bubble contraction (scrunching or antiscrunching).

scholarly journals Bromo- and Extraterminal Domain Chromatin Regulators Serve as Cofactors for Murine Leukemia Virus Integration

2013 ◽  
Vol 87 (23) ◽  
pp. 12721-12736 ◽  
Author(s):  
Saumya Shree Gupta ◽  
Tobias Maetzig ◽  
Goedele N. Maertens ◽  
Azar Sharif ◽  
Michael Rothe ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Retroviral Vectors ◽  
Transcription Start ◽  
Preintegration Complex ◽  
Transcription Start Sites ◽  
Bet Inhibitors ◽  
Murine Leukemia

Retroviral integrase (IN) proteins catalyze the permanent integration of proviral genomes into host DNA with the help of cellular cofactors. Lens epithelium-derived growth factor (LEDGF) is a cofactor for lentiviruses, including human immunodeficiency virus type 1 (HIV-1), and targets lentiviral integration toward active transcription units in the host genome. In contrast to lentiviruses, murine leukemia virus (MLV), a gammaretrovirus, tends to integrate near transcription start sites. Here, we show that the bromodomain and extraterminal domain (BET) proteins BRD2, BRD3, and BRD4 interact with gammaretroviral INs and stimulate the catalytic activity of MLV INin vitro. We mapped the interaction site to a characteristic structural feature within the BET protein extraterminal (ET) domain and to three amino acids in MLV IN. The ET domains of different BET proteins stimulate MLV integrationin vitroand, in the case of BRD2, alsoin vivo. Furthermore, two small-molecule BET inhibitors, JQ1 and I-BET, decrease MLV integration and shift it away from transcription start sites. Our data suggest that BET proteins might act as chromatin-bound acceptors for the MLV preintegration complex. These results could pave a way to redirecting MLV DNA integration as a basis for creating safer retroviral vectors.

scholarly journals Comparison between Protoplast Transformation and Co-transformation in `Hamlin' Sweet Orange [Citrus sinensis (L.) Osbeck]

HortScience ◽  
2006 ◽  
Vol 41 (4) ◽  
pp. 972D-973
Author(s):  
Ahmad A. Omar ◽  
Wen-Yuan Song ◽  
James H. Graham ◽  
Jude W. Grosser
Keyword(s):  
Transgenic Plants ◽  
Citrus Sinensis ◽  
Fluorescent Protein ◽  
Sweet Orange ◽  
Citrus Canker ◽  
Yield Potential ◽  
High Yield ◽  
Pcr Analysis ◽  
Dna Encoding ◽  
Early Maturity

Citrus canker disease caused by the bacterial pathogen Xanthomonas axonopodis pv. citri is becoming a worldwide problem. Xa21 gene is a member of the Xa21 gene family of rice, which provides broad spectrum Xanthomonas resistance in rice. `Hamlin' sweet orange [Citrus sinensis (L.) Osbeck) is one of the leading commercial cultivars in Florida because of its high yield potential and early maturity. `Hamlin' also has a high regeneration capacity from protoplasts and is often used in transformation experiments. Since the citrus canker pathogen is in the same genus, this gene may have potential to function against canker in citrus. The wild-type Xa21 gene contains an intron, and there are some questions whether dicot plants can process genes containing monocot introns (the cDNA is intron-free). Plasmids DNA, encoding the non-destructive selectable marker EGFP (Enhanced Green Fluorescent Protein) gene and the cDNA of the Xa21 gene were transformed or co-transformed into `Hamlin' orange protoplasts using polyethylene glycol. More than 200 transgenic embryoids were recovered. More than 400 transgenic plants were developed from 75 independent transgenic events. PCR analysis revealed the presence of the cDNA of the Xa21 and the GFP genes in the transgenic plants. Some of the plants have the GFP only. Southern analysis is showing integration of the cDNA into different sites ranges from one to five sites. Western analysis is showing the expression of the cDNA of the Xa21 gene in the transgenic citrus plants. This is the first time that a gene from rice has been stably integrated and expressed in citrus plants. Canker challenge assay is in progress.

scholarly journals Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6/TAK1/MAPK and Nrf2 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Hai-han Liao ◽  
Nan Zhang ◽  
Yan-yan Meng ◽  
Hong Feng ◽  
Jing-jing Yang ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Mapk Signaling ◽  
Neonatal Rat ◽  
Mouse Heart ◽  
Pathological Cardiac Hypertrophy ◽  
Pathological Hypertrophy ◽  
Nrf2 Signaling Pathway

Myricetin (Myr) is a common plant-derived polyphenol and is well recognized for its multiple activities including antioxidant, anti-inflammation, anticancer, and antidiabetes. Our previous studies indicated that Myr protected mouse heart from lipopolysaccharide and streptozocin-induced injuries. However, it remained to be unclear whether Myr could prevent mouse heart from pressure overload-induced pathological hypertrophy. Wild type (WT) and cardiac Nrf2 knockdown (Nrf2-KD) mice were subjected to aortic banding (AB) surgery and then administered with Myr (200 mg/kg/d) for 6 weeks. Myr significantly alleviated AB-induced cardiac hypertrophy, fibrosis, and cardiac dysfunction in both WT and Nrf2-KD mice. Myr also inhibited phenylephrine- (PE-) induced neonatal rat cardiomyocyte (NRCM) hypertrophy and hypertrophic markers’ expression in vitro. Mechanically, Myr markedly increased Nrf2 activity, decreased NF-κB activity, and inhibited TAK1/p38/JNK1/2 MAPK signaling in WT mouse hearts. We further demonstrated that Myr could inhibit TAK1/p38/JNK1/2 signaling via inhibiting Traf6 ubiquitination and its interaction with TAK1 after Nrf2 knockdown in NRCM. These results strongly suggested that Myr could attenuate pressure overload-induced pathological hypertrophy in vivo and PE-induced NRCM hypertrophy via enhancing Nrf2 activity and inhibiting TAK1/P38/JNK1/2 phosphorylation by regulating Traf6 ubiquitination. Thus, Myr might be a potential strategy for therapy or adjuvant therapy for malignant cardiac hypertrophy.

Production of sweet orange somaclones tolerant to citrus canker disease by in vitro mutagenesis with EMS

2015 ◽  
Vol 123 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Hongjuan Ge ◽  
Yi Li ◽  
Hongyan Fu ◽  
Guiyou Long ◽  
Li Luo ◽  
...  
Keyword(s):  
Sweet Orange ◽  
Citrus Canker ◽  
In Vitro Mutagenesis ◽  
Canker Disease ◽  
Citrus Canker Disease

Transformation of sweet orange [Citrus sinensis (L.) Osbeck] with pthA-nls for acquiring resistance to citrus canker disease

2010 ◽  
Vol 75 (1-2) ◽  
pp. 11-23 ◽  
Author(s):  
Li Yang ◽  
Chunhua Hu ◽  
Na Li ◽  
Jiayin Zhang ◽  
Jiawen Yan ◽  
...  
Keyword(s):  
Citrus Sinensis ◽  
Sweet Orange ◽  
Citrus Canker ◽  
Canker Disease ◽  
Citrus Canker Disease

In vitro and in vivo activity of QoI fungicides against Colletotrichum gloeosporioides causing fruit anthracnose in Citrus sinensis

2018 ◽  
Vol 236 ◽  
pp. 90-95 ◽  
Author(s):  
Giulio Piccirillo ◽  
Raffaele Carrieri ◽  
Giancarlo Polizzi ◽  
Antonino Azzaro ◽  
Ernesto Lahoz ◽  
...  
Keyword(s):  
Citrus Sinensis ◽  
Colletotrichum Gloeosporioides ◽  
Qoi Fungicides

scholarly journals Evaluation of Resistance to Asiatic Citrus Canker among Selections of Pêra Sweet Orange (Citrus sinensis)

Plant Disease ◽  
2016 ◽  
Vol 100 (10) ◽  
pp. 1994-2000 ◽  
Author(s):  
Aline M. O. Gonçalves-Zuliani ◽  
Danielle S. Y. Nanami ◽  
Bruna R. Barbieri ◽  
Terezinha A. Guedes ◽  
Carlos A. Zanutto ◽  
...  
Keyword(s):  
Host Resistance ◽  
Citrus Sinensis ◽  
Field Experiments ◽  
Sweet Orange ◽  
Citrus Canker ◽  
Leaf Miner ◽  
Citrus Leaf ◽  
Greenhouse Experiments ◽  
Lesion Diameter ◽  
Mesophyll Resistance

Asiatic citrus canker (ACC, caused by the bacterium Xanthomonas citri subsp. citri) is a destructive disease of citrus in Brazil and in several other citrus-producing countries. ACC management is problematic, and bactericides such as copper can be reasonably efficacious but do not completely control the disease. Furthermore, injury by citrus leaf miner (CLM) can exacerbate severity of ACC. Host resistance is the most desirable solution for management of ACC; however, evaluations of germplasm indicate that resistance is limited in many popular species and cultivars that are grown commercially. Limited evaluations have been made of sweet orange (Citrus sinensis) selections. We evaluated resistance of 25 Pêra sweet orange selections to X. citri subsp. citri by wound inoculation and measuring lesion diameter under greenhouse conditions (wound inoculation indicates mesophyll resistance which will be valuable in areas where CLM exists). ACC severity was assessed on the same 25 selections at three locations in the field in Brazil, relying on natural inoculum and conditions to cause disease. In the greenhouse experiments, the selections EEL, Bianchi/CC, Ipiguá, Olimpia, IAC 2000/1, and Ovale Siracusa consistently had the smallest diameter lesions, indicating greatest resistance, although differences in lesion diameter were small. Results from the field experiments were less conclusive, although EEL and Ovale Siracusa were consistently numerically least affected by ACC. These results indicate selections of sweet orange that might be preferable to consider in canker-prone areas in Brazil and elsewhere.

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