5 research outputs found
Effects of herbicides on fungal phytopathogens
Herbicides are inevitable inputs to control excessive weed in crop land, particularly where modern agricultural practices such as conservation tillage, are opted. Intensive farming has increased the market value of herbicides among the other pesticides. Although herbicides are effective in controlling weed population, administration of this synthetic chemicals may alter the soil microbial community causing potential increase of plant pathogens. Moreover, herbicides may also have nontarget effects on the cultivated crops making them more susceptible to diseases. Actions of herbicides in soil that either stimulate microbial growth or wipe out some microbial population may create space for the thrivial of opportunistic fungi. Previous studies showed that white rot fungi are more tolerant to herbicides as they produce lignin degrading enzymes that are highly oxidative, non-specific and are able to transform a wide range of herbicides. Besides that, this group of fungi can grow on agricultural waste substrates. Influence of these herbicides on soil microbial ecosystem and interactions of plants and pathogenic white rot fungi modulate disease development in plant hosts
Effects of herbicides, hydrogen peroxide and phytohormones on Ganoderma infection in oil palm (Elaeis guineensis Jacq.) roots
Basal Stem Rot (BSR) caused by Ganoderma is the major disease that infects oil palms (Elaeis
guineensis Jacq.). Application of herbicides in plantations for weed control might affect
BSR development. The effects of hydrogen peroxide (H2O2) and phytohormones which are key
signalling agents in plant defense mechanisms on Ganoderma infection are unknown. Therefore,
the objectives of this study are to investigate the effects of herbicides, H2O2 and phytohormones
on Ganoderma infection in oil palm roots, and to profile the gene expression of transcripts related
to hydrogen peroxide production, hormone biosynthesis and signaling during Ganoderma infection
in oil palm roots. The effects of three commonly used herbicides in plantations on the
growth of Ganoderma spp. and infection progress in G. boninense PER71-inoculated oil palm
seedlings were examined. Evaluation on the tolerance of G. boninense (pathogenic),
G. miniatocinctum (pathogenic), and G. lucidum (non-pathogenic) to herbicides revealed
that glyphosate (Roundup®, GLY) 1800 ppm-2700 ppm can reduce the growth of all three Ganoderma
species. Both Basta (GLA at 750-3000 ppm) and Paraquat (PQ at 325-300 ppm) inhibited the
growth of all three Ganoderma species studied except for G. lucidum which was able to grow at
650 ppm PQ. GLA and PQ increased the disease severity of oil palm to Ganoderma infection. The
fungus may avoid the herbicide contaminated soil environment and then infected the oil
palm seedlings that could have been weakened by the herbicides. The open reading
frame and conserved functional domains of eight cDNAs encoding H2O2, phytohormone biosynthesis
and signalling in oil palm were analyzed. The transcript abundance of EgRBOHB2 in G.
boninense-treated oil palm roots increased 2.42 fold at 3 wpi compared to uninoculated
oil palm seedlings. Meanwhile, EgRBOHB1, EgRBOHH and EgHIR did not show
significant changes in expression at all three time points. The transcript
abundance of EgCOI (jasmonic acid, JA-related) increased at 6 and 12 wpi whereas the
transcript abundance EgNPR1 (salicyclic acid, SA-related) increased at 3 wpi, reduced at 6 and 12 wpi; suggesting a well-coordinated signal
crosstalk between JA and SA. The expression of EgOPR which is related to JA biosynthesis was
up-regulated at 6 wpi; coincided with the upregulation of EgCOI (which perceives JA). The
EgACO1 (ethylene, ET- related) was also upregulated at the early stage of infection by 3.2 and
2.2 fold at 3 and 6 wpi in the inoculated oil palm seedlings, respectively. The exogenous
application of phytohormones did not suppress the BSR in Ganoderma-inoculated oil palm
seedlings while the application of their inhibitors, caused an early onset and more
severe disease symptoms. DPI pre-treatment was the only treatment that delayed the onset and
reduced the severity of disease symptoms. The distilled water-treated Ganoderma inoculated oil
palm fresh root samples (control) had a significantly higher H2O2 level at 3 wpi compared with
uninoculated oil palm root samples. However, there was no significant difference in H2O2 level
between the Ganoderma inoculated and uninoculated oil palm root sample of the other
phytohormone-treated or their inhibitor treated oil palm seedlings. The JA-treated and
Ganoderma-inoculated oil palm root sample had the lowest H2O2 level among all the
other roots samples at 6 wpi while the SA-treated, Ganoderma inoculated oil palm roots
had the lowest H2O2 level among all the other root samples at 12 wpi. The H2O2 inhibitor-
treated oil palm roots generally had lower H2O2 level when compared with other treatments.
Overall, the H2O2 levels did not correspond to the disease symptoms and severity but showed an
increase at the onset of disease symptoms. In conclusion, the findings from this study
have given an insight on the effects of herbicides, H2O2, phytohormones and their
inhibitors on Ganoderma infection and disease progress of BSR in oil palm
seedlings
Temporal expression of defense-related genes in Ganoderma-infected oil palm roots
Basal stem rot is an oil palm disease which causes substantial loss to the oil palm industry in Southeast Asia. Temporal gene expression analysis of oil palms infected with Ganoderma boninense is important to identify the defense pathways at biotrophic and necrotrophic phases of fungal infection. The aim of this study was to analyze the gene expression of oil palm genes related to respiratory burst oxidation, phytohormone biosynthesis, salicylic acid- and jasmonic acid-mediated defense pathways in oil palm roots infected by G. boninense at different time points. The findings of this study confirmed that salicylic acid mediated the early defense response from infected oil palm during the biotrophic phase of fungal infection, while the JA-mediated defense response was triggered when the root lesions occurred in the infected oil palm root tissues during the necrotrophic phase of Ganoderma infection. The oil palm defense responses may play a role in delaying the progression of basal stem rot but is insufficiently effective to eradicate Ganoderma infection. Temporal gene expression may help in finding methods to ameliorate the impact of basal stem rot by prolonging the productive lifespan of diseased trees and to reduce the economic loss due to this disease