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1.
Plant Dis ; 2024 May 19.
Artículo en Inglés | MEDLINE | ID: mdl-38764336

RESUMEN

Kousa dogwood (Cornus kousa) is an economically important woody ornamental crop that exhibits creamy, white, pointed bracts in late spring, and reddish to pink drupe fruits in late summer and fall. It bears shiny dark green leaves that become reddish-purple to scarlet in the fall. In August of 2023, 3-year-old container grown C. kousa var. chinensis plants in a commercial nursery in Warren Co., Tennessee, exhibited severe yellowing, dieback and root rot symptoms (Fig. 1a and 1b). Dark brown to black lesions were observed in the root and crown region of the plants. Disease severity was 40% to 60% of root area affected, and disease incidence was approximately 40% of 1,000 plants. Surface-sterilized (10% NaOCl: 1 min) symptomatic root tissues were plated on V8-PARPH and incubated at 25°C. Sparse aerial mycelium, showing a distinct rosette or faint radiate to chrysanthemum colony pattern, was observed within four days of incubation (Fig. 2). All isolates produced ovoid or subglose, papillate, and proliferating sporangia in grass blade water cultures (Dervis et al. 2020). Sporangia measured as 19.18 to 24.80 µm X 18.08 to 22.16 µm (n = 50) with a length/width ratio of 1.06 to 1.11. Zoospores observed were between 7.07 to 9.98 µm in diameter (n = 50). Oogonia and oospores were not produced. The ribosomal internal transcribed spacer (ITS) and large subunit (LSU), as well as mitochondrial cytochrome oxidase subunit II (COX-II) genetic markers were amplified and sequenced using primer pairs ITS1/ITS4 (White et al. 1990), NL1/NL4 (Baten et al. 2014), and cox2-F/cox2-RC4 (Choi et al. 2015), respectively. The ITS, LSU, and COX-II sequences of isolates FBG6343, FBG6344 (ITS: PP458373 and PP461387; LSU: PP461390 and PP461391; COXII: PP477112 and PP477113) were 100% identical to those of MN306118, HQ643386, and MN206732, respectively. Based on the morphology (Nechwatal and Mendgen 2006) and sequence data, the isolates were identified as Phytopythium litorale (Nechw.) Abad, De Cock, Bala, Robideau, Lodhi & Lévesque. The pathogenicity test was performed on 3-year-old C. kousa var. chinensis plants grown in a 3-gal container to fulfill Koch's postulates. Kousa dogwood plants were drench inoculated (800 ml/plant) with a pathogen slurry (two plates of 7-day-old culture/liter) of isolates FBG6343 and FBG6364 (five plants per isolate). Control plants were drenched with agar slurry without the pathogen. The study was conducted in a greenhouse maintained at 21 to 23°C and 70% relative humidity with a 16-h photoperiod and irrigated twice a day for 2 min using an overhead irrigation system. Forty-five days after inoculation, plants showed dieback symptoms, and dark brown lesions developed in the roots of all inoculated plants. Isolates with morphology and sequences identical to those of FBG6343 and FBG6364 were recovered from root tissues of all inoculated plants. All control plants remained symptom-free, and P. litorale was not isolated from the root tissue. Previously, P. litorale was reported to cause disease on apple, kiwi, planatus, and rhododendron (Dervis et al. 2020; Li et al. 2021; Mert et al. 2020; Polat et al. 2023). To our knowledge, this is the first report of P. litorale causing root rot of kousa dogwood in Tennessee and the United States. Identification of this pathogen as the causal agent is crucial to developing timely management practices.

2.
Nat Commun ; 13(1): 7168, 2022 11 22.
Artículo en Inglés | MEDLINE | ID: mdl-36418866

RESUMEN

CRISPR-Cas mediated genome engineering has revolutionized functional genomics. However, understanding of DNA repair following Cas-mediated DNA cleavage remains incomplete. Using Cas12a ribonucleoprotein genome editing in the fungal pathogen, Magnaporthe oryzae, we detail non-canonical DNA repair outcomes from hundreds of transformants. Sanger and nanopore sequencing analysis reveals significant variation in DNA repair profiles, ranging from small INDELs to kilobase size deletions and insertions. Furthermore, we find the frequency of DNA repair outcomes varies between loci. The results are not specific to the Cas-nuclease or selection procedure. Through Ku80 deletion analysis, a key protein required for canonical non-homologous end joining, we demonstrate activity of an alternative end joining mechanism that creates larger DNA deletions, and uses longer microhomology compared to C-NHEJ. Together, our results suggest preferential DNA repair pathway activity in the genome that can create different mutation profiles following repair, which could create biased genome variation and impact genome engineering and genome evolution.


Asunto(s)
Sistemas CRISPR-Cas , Roturas del ADN de Doble Cadena , Sistemas CRISPR-Cas/genética , Mutación , ADN/genética
3.
Plants (Basel) ; 9(9)2020 Sep 09.
Artículo en Inglés | MEDLINE | ID: mdl-32916856

RESUMEN

Plant-parasitic nematodes (PPN) are among the most economically and ecologically damaging pests, causing severe losses of crop production worldwide. Chemical-based nematicides have been widely used, but these may have adverse effects on human health and the environment. Hence, biological control agents (BCAs) have become an alternative option for controlling PPN, since they are environmentally friendly and cost effective. Lately, a major effort has been made to evaluate the potential of a commercial grade strain of plant growth-promoting rhizobacteria (PGPR) as BCAs, because emerging evidence has shown that PGPR can reduce PPN in infested plants through direct and/or indirect antagonistic mechanisms. Direct antagonism occurs by predation, release of antinematicidal metabolites and semiochemicals, competition for nutrients, and niche exclusion. However, the results of direct antagonism may be inconsistent due to unknown endogenous and exogenous factors that may prevent PGPR from colonizing plant's roots. On the other hand, indirect antagonism may occur from the induced systemic resistance (ISR) that primes whole plants to better fight against various biotic and abiotic constraints, actuating faster and/or stronger defense responses (adaption), enhancing their promise as BCAs. Hence, this review will briefly revisit (i) two modes of PGPR in managing PPN, and (ii) the current working models and many benefits of ISR, in the aim of reassessing current progresses and future directions for isolating more effective BCAs and/or developing better PPN management strategy.

4.
Am J Case Rep ; 20: 248-251, 2019 Feb 25.
Artículo en Inglés | MEDLINE | ID: mdl-30799434

RESUMEN

BACKGROUND Medications are one of the most common causes of acute kidney injury (AKI). Elderly patients with diabetes mellitus and chronic kidney disease seem to be at particularly high risk for development of medication-induced AKI. Among antibiotics, the most commonly implicated agents are aminoglycosides, cephalosporins, trimethoprim-sulfamethoxazole, acyclovir, and amphotericin. Despite its widespread use, clindamycin has been rarely associated with AKI. CASE REPORT A 52-year-old male patient with type II insulin dependent diabetes mellitus without diabetic nephropathy was treated with clindamycin for chronic osteomyelitis. Five days following initiation of therapy, he developed nausea, poor appetite, decrease in urine output, and profound generalized weakness. His symptoms were initially attributed to gastrointestinal side effects of clindamycin and he was advised to take it with food and to hydrate himself vigorously. Despite this change, his symptoms progressed and he developed hematuria and AKI which prompted hospital admission. Extensive workup for AKI that included evaluation for pre-renal, intrinsic renal, and post-renal etiologies failed to point to other etiologies apart from clindamycin-induced AKI. Following cessation of medication and temporary renal replacement therapy (RRT), his renal function returned to baseline. CONCLUSIONS We present a case of clindamycin-induced AKI that was diagnosed after a delay due to uremia symptoms being mistakenly attributed to gastrointestinal side effects of clindamycin. Although rare, clindamycin can be a cause of AKI and clinician should be aware of this association in order to recognize and treat it in timely manner.


Asunto(s)
Lesión Renal Aguda/etiología , Antibacterianos/efectos adversos , Clindamicina/efectos adversos , Humanos , Masculino , Persona de Mediana Edad , Osteomielitis/tratamiento farmacológico
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