Corrigendum: Expression of Pumpkin Gene Improves Powdery Mildew Resistance in Tobacco.

[This corrects the article DOI: 10.3389/fpls.2020.

Expression of Pumpkin Gene Improves Powdery Mildew Resistance in Tobacco.

Powdery mildew (PM), caused by , is a major threat to the global cucurbit yield. The molecular mechanisms underlying the PM resistance of pumpkin ( Duch.) are largely unknown.

Improved Powdery Mildew Resistance of Transgenic Overexpressing the Gene.

Powdery mildew (PM), which is mainly caused by , is a serious biotrophic pathogen disease affecting field-grown and greenhouse-grown cucurbit crops worldwide. Because fungicides poorly control PM, the development and cultivation of PM-resistant varieties is critical. A homolog of (), which encodes a key component of the plant disease-associated signal transduction pathway, was previously identified through a transcriptomic analysis of a PM-resistant pumpkin () inbred line infected with PM.

[Effects of NaCl stress on free polyamines content and reactive oxygen species level in pumpkin roots].

Taking Cucurbita moschata Duch hybrid 360-3 x 112-2 and C. ficifolia Bouche as test materials, the effects of NaCl stress on their plant growth and the O2*- production rate and H2O2 and free polyamines (PAs) contents in their roots were studied with hydroponic culture. The results showed that after 10 d NaCl stress, the plant growth of the two pumpkin varieties was strongly inhibited, compared with the control, and C.

Species-specific transcriptional activity of synthetic flavonoids in guinea pig and mouse cells as a result of differential activation of the aryl hydrocarbon receptor to interact with dioxin-responsive elements.

To investigate possible species-specificity of aryl hydrocarbon receptor (AhR)-mediated signal transduction pathways, activities of 2,3,7,8-tetrochlorodibenzo-p-dioxin (TCDD) and six synthetic flavonoids were evaluated in mouse hepatoma and guinea pig adenocarcinoma cells transfected with an AhR-responsive luciferase reporter. Rank order potency in these two cell lines was similar for the ability of these flavonoids to antagonize TCDD-induced reporter gene expression. However, in the presence of flavone alone, a species-specific difference in agonist activity was observed.