Biocontrol of citrus fungal pathogens by lipopeptides produced by TZ01.

Citrus diseases caused by fungal pathogens drastically decreased the yield and quality of citrus fruits, leading to huge economic losses. Given the threats of chemical pesticides on the environment and human health, biocontrol agents have received considerable attention worldwide as ecofriendly and sustainable alternative to chemical fungicides. In the present study, we isolated a strain TZ01 with potent antagonistic effect against three citrus pathogenic fungi: , and The culture supernatant of this strain exhibited remarkable antifungal activity on potato dextrose agar plates and detached leaves of five citrus varieties.

RNA interference of PHB1 enhances virulence of Vip3Aa to Sf9 cells and Spodoptera frugiperda larvae.

Background: In our previous work, we demonstrated that prohibitin 2 (PHB2) on the membrane of Sf9 cells was a receptor for Vip3Aa, and PHB2 in mitochondria contributed to the mitochondrial stability to reduce Vip3Aa toxicity. Prohibitin 1 (PHB1), another prohibitin family member, forms heterodimers with PHB2 to maintain the structure and stability of mitochondria. To explore whether PHB1 impacts the action process of Vip3Aa, we examined the correlation between PHB1 and Vip3Aa virulence.

Vegetative Insecticidal Protein Vip3Aa Is Transported via Membrane Vesicles in BMB171.

Vegetative insecticidal protein Vip3Aa, secreted by many (Bt) strains during the vegetative growth stage, represents the second-generation insecticidal toxin. In recent years, significant progress has been made on its structure and action mechanism. However, how it is translocated across the cytoplasmic membrane into the environment remains a mystery.

NupR Responding to Multiple Signals Is a Nucleoside Permease Regulator in Bacillus thuringiensis BMB171.

Nucleoside transport is essential for maintaining intracellular nucleoside and nucleobase homeostasis for living cells. Here, we identified an uncharacterized GntR/HutC family transcriptional regulator, NagR2, renamed NupR (nucleoside permease regulator), that mainly controls nucleoside transport in the Bacillus thuringiensis BMB171 strain. The deletion or overexpression of affected the bacteria's utilization of guanosine, adenosine, uridine, and cytidine rather than thymidine.

PHB2 affects the virulence of Vip3Aa to Sf9 cells through internalization and mitochondrial stability.

The vegetative insecticidal proteins (Vip3A) secreted by some (Bt) strains during vegetative growth are regarded as a new generation of insecticidal toxins. Like insecticidal crystal proteins, they are also used in transgenic crops to control pests. However, their insecticidal mechanisms are far less defined than those of insecticidal crystal protein.

Attenuator LRR - a regulatory tool for modulating gene expression in Gram-positive bacteria.

With the rapid development of synthetic biology in recent years, particular attention has been paid to RNA devices, especially riboswitches, because of their significant and diverse regulatory roles in prokaryotic and eukaryotic cells. Due to the limited performance and context-dependence of riboswitches, only a few of them (such as theophylline, tetracycline and ciprofloxacin riboswitches) have been utilized as regulatory tools in biotechnology. In the present study, we demonstrated that a ribosome-dependent ribo-regulator, LRR, discovered in our previous work, exhibits an attractive regulatory performance.

Autophagy induced by Vip3Aa has a pro-survival role in Sf9 cells.

Vip3Aa is an insecticidal protein that can effectively control certain lepidopteran pests and has been used widely in biological control. However, the mechanism of action of Vip3Aa is unclear. In the present study, we showed that Vip3Aa could cause autophagy in Sf9 cells, which was confirmed by the increased numbers of GFP-Atg8 puncta, the appearance of autophagic vacuoles, and an elevated Atg8-II protein level.

Mitochondria and Lysosomes Participate in Vip3Aa-Induced Sf9 Cell Apoptosis.

Vip3Aa, a soluble protein produced by certain strains, is capable of inducing apoptosis in Sf9 cells. However, the apoptosis mechanism triggered by Vip3Aa is unclear. In this study, we found that Vip3Aa induces mitochondrial dysfunction, as evidenced by signs of collapse of mitochondrial membrane potential, accumulation of reactive oxygen species, release of cytochrome c, and caspase-9 and -3 activation.