|Xu, Junhuan -|
Submitted to: Insect Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 5, 2012
Publication Date: April 22, 2012
Citation: Xu, J., James, R.R. 2012. Temperature stress affects the expression of immune response genes in the alfalfa leafcutting bee (Megachile rotundata). Insect Molecular Biology. 21(2): 269-280. Interpretive Summary: Chalkbrood is a disease of bees caused by a fungal pathogen. Previously, it has always been thought that “chilled brood” are more susceptible to chalkbrood than brood kept at the normally high temperature of a honey bee hive (approximately 35 C). The effect of chilling on chalkbrood levels has been experimentally demonstrated in honey bees, the alfalfa leafcutting bee, and the blue orchard bee. However, by testing a wider range of temperatures than previously tested, we demonstrate that it is actually intermediate temperatures that cause increases in chalkbrood, at least for the alfalfa leafcutting bee, and chalkbrood is a very important disease in this bee. Using molecular techniques, we found that both high and low temperature stresses increased bee immune responses and decreased disease. In addition, the pathogen manipulated the bee’s physiology. In particular, it affected protein synthesis, but differently at different temperatures, with the lowest rates of protein synthesis occurring at 30°C (the temperature with the highest infection rates). We hypothesize that temperature stress, especially high temperature stress, heightens the insect immune response before the pathogen triggers an immune reaction in the host, and this early activity prevents infection.
Technical Abstract: The alfalfa leafcutting bee (Megachile rotundata) is affected by a fungal disease called chalkbrood. In several species of bees, chalkbrood is more likely to occur in larvae kept at 25-30 C than at 35 C. We found that both high and low temperature stress increased the expression of immune response genes in the alfalfa leafcutting bee, and thus increased disease resistance. Genes associated with pathogen recognition and trypsin-like serine proteases were most highly expressed at the lowest rearing temperature (20 C), while prophenoloxidase, melanization, immune response signalling pathways, effectors, and reactive oxygen species were most highly expressed at the warmest temperature (35 C). In addition, the pathogen appears to be able to affect other host functions, particularly protein synthesis, but differentially at different temperatures, with the lowest rates of protein synthesis occurring at 30°C. We hypothesize that temperature stress heightens the insect immune response before the pathogen has elicited a response in the host, and it is this early activity that prevents infection.