Abstract
Phosphine is the only general use fumigant for the protection of stored grain, though its long-term utility is threatened by the emergence of highly phosphine-resistant pests. Given this precarious situation, it is essential to identify factors, such as stress preconditioning, that interfere with the efficacy of phosphine fumigation. We used Caenorhabditis elegans as a model organism to test the effect of pre-exposure to heat and cold shock, UV and gamma irradiation on phosphine potency. Heat shock significantly increased tolerance to phosphine by 3-fold in wild-type nematodes, a process that was dependent on the master regulator of the heat shock response, HSF-1. Heat shock did not, however, increase the resistance of a strain carrying the phosphine resistance mutation, dld-1(wr4), and cold shock did not alter the response to phosphine of either strain. Pretreatment with the LD50 of UV (18 J cm-2) did not alter phosphine tolerance in wild-type nematodes, but the LD50 (33 J cm-2) of the phosphine resistant strain (dld-1(wr4)) doubled the level of resistance. In addition, exposure to a mild dose of gamma radiation (200 Gy) elevated the phosphine tolerance by ~2-fold in both strains.
Highlights
Phosphine (PH3) gas is an ideal fumigant for the control of insect pests of stored commodities due to the low cost of application, ease of use and the lack of chemical residues
The effect of physical pre-conditioning on phosphine toxicity modified heat shock response, The three strains, (RB791, RB1104 and PS3551), were provided by the C. elegans Genetic center (CGC), which is funded by the National Institutes of Health (NIH) Office of Research Infrastructure Programs (P40 OD010440)
We tested the ability of four distinct stresses to induce cross-resistance against the agriculturally important fumigant phosphine, with the goal of gaining a deeper understanding of how resistance is mediated
Summary
Phosphine (PH3) gas is an ideal fumigant for the control of insect pests of stored commodities due to the low cost of application, ease of use and the lack of chemical residues. Phosphine is environmentally benign as it decomposes to phosphate. These properties are not matched by any other potential fumigant, leading to heavy dependence on phosphine fumigation around the world [1]. Phosphine is a metabolic poison that affects cellular respiration [2, 3]. It may disrupt neural acetylcholine signaling [4] or cause damage to DNA [5]. Phosphine is known to cause oxidative damage [4]. The diversity of potential mechanisms makes it difficult to predict interactions between phosphine and other treatments
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