摘要
Griffonia simplicifolia lectin II （GSII） and wheat germ agglutinin （WGA） are N-acetylglucosamine-binding lectins. Previous studies demonstrated that they have anti- insect activity, a property potentially useful in pest control. To gain some insight into the insect response to dietary lectins, we performed transcriptomic analysis using the cowpea bruchid （Callosobruchus maculatus） midgut microarray platform we built. Compared to the normutritional cellulose treatment, dietary lectins induced more profound changes in gene expression. Ingestion of relatively high doses oflectins for 24 h resulted in alteration of gene expression involved in sugar and lipid metabolism, transport, development, defense, and stress tolerance. Metabolic genes were largely downregulated. Moreover, we observed disorganized microvilli resulting from ingestion of WGA. This morphological change is consistent with the lectin-induced changes in genes related to midgut epithelial cell repair. In addition, suboptimal nutrient conditions may serve as a stress signal to trigger senescence processes, leading to growth arrest and developmental delay.
Griffonia simplicifolia lectin II （GSII） and wheat germ agglutinin （WGA） are N-acetylglucosamine-binding lectins. Previous studies demonstrated that they have anti- insect activity, a property potentially useful in pest control. To gain some insight into the insect response to dietary lectins, we performed transcriptomic analysis using the cowpea bruchid （Callosobruchus maculatus） midgut microarray platform we built. Compared to the normutritional cellulose treatment, dietary lectins induced more profound changes in gene expression. Ingestion of relatively high doses oflectins for 24 h resulted in alteration of gene expression involved in sugar and lipid metabolism, transport, development, defense, and stress tolerance. Metabolic genes were largely downregulated. Moreover, we observed disorganized microvilli resulting from ingestion of WGA. This morphological change is consistent with the lectin-induced changes in genes related to midgut epithelial cell repair. In addition, suboptimal nutrient conditions may serve as a stress signal to trigger senescence processes, leading to growth arrest and developmental delay.
基金
Acknowledgments We thank Dr. Ron Salzman for his critical review of this manuscript. This project was supported by the USDA National Research Initiative grant# 2005-35604-15438, by the Natural Science Foundation of Jiangsu Province （BK20130711）, and by Basic Science Research Program through the NRF of Korea funded by the MOEST （2012R1A1A2044114）.
