Effects of carbendazim on conidial germination and mitosis in germlings ofFusarium graminearumandBotrytis cinerea

Abstract

The effects of carbendazim on carbendazim-sensitive (wild-type) and -resistant strains of Fusarium graminearum and Botrytis cinerea were compared. When treated with carbendazim, conidia and germlings of wild-type F. graminearum and B. cinerea germinated and grew to produce stunted, distorted, and abnormally branched germlings; in addition, distinct nuclei were replaced by irregularly distributed chromosome masses, and normal nuclear division was not observed. The CMI (chromosome mitosis index) values of wild-type strains rapidly increased within 60 min of treatment with carbendazim and then rapidly declined. Whereas the wild-type strains of the two fungi responded similarly, the carbendazim-resistant strains of F. graminearum and B. cinerea responded differently to carbendazim. The resistant strain of F. graminearum showed normal mitosis but produced significantly more branches and higher CMI values when treated with carbendazim than when untreated. In contrast, the carbendazim-resistant strain of B. cinerea exhibited normal morphology and mitosis after carbendazim treatment. The results suggest that the mechanism for carbendazim resistance in F. graminearum differs from that in B. cinerea and other fungi.

Involvement of FgMad2 and FgBub1 in regulating fungal development and carbendazim resistance in Fusarium graminearum

“…In yeast cells, treatment of the wild type with benzimidazole‐related microtubule inhibitors leads to cell cycle arrest in mitosis (Roberts et al ., ), and the same phenomenon has been documented in F. graminearum (Bi et al ., ). Therefore expression levels of the two SAC genes relative to those of the parental isolates were investigated after treatment of F. graminearum isolates with MBC.…”

“…The above research demonstrates that F. graminearum was weakened in defence against microtubule disruption agents when Mad2 or Bub1 was impaired. According to previous research, MBC principally interacts with b 2 -tubulin of F. graminearum and suppresses survival by interfering with mitosis (Bi et al, 2009). The amino acid mutations in key Plant Pathology (2015) 64, 1014-1028 locations of b 2 -tubulin confer different levels of resistance to MBC.…”

Antifungal Metabolite p-Aminobenzoic Acid (pABA): Mechanism of Action and Efficacy for the Biocontrol of Pear Bitter Rot Disease

“…9 The main defense against fungal pear pathogens consists of the use of synthetic fungicides, such as carbendazim or thiabendazole, which arrest the fungal cell cycle, and thus pathogen growth. 10 Fungi habitually produce asexual spores, called conidia, which germinate in the presence of favorable substrates, such as sugars and amino acids. 11,12 Then, formation of the germ tube, DNA replication, and septation steps take place, allowing for the formation of new cells and thus fungal expansion.…”

Fungicide: Modes of Action and Possible Impact on Nontarget Microorganisms

“…They can also influence the beneficial arbuscular mycorrhiza fungi (AMF) [30] and mammalian cells [65,66]. Although no evidence of a direct effects of MBC fungicides on soil bacteria was reported yet, some research has associated these fungicides to the inhibition of nitrification in soil, a microbially mediated process [29].…”