RESUMEN
Common smut, caused by Ustilago maydis (DC.) Corda, is a destructive fungal disease of maize worldwide; it forms large tumors, reducing corn yield and quality. However, the molecular defense mechanism to common smut in maize remains unclear. The present study aimed to use a leading maize inbred line Ye478 to analyze the response to U. maydis inoculation. The histological and cytological analyses demonstrated that U. maydis grew gradually to the host cells 6 h post-inoculation (hpi). The samples collected at 0, 3, 6, and 12 hpi were analyzed to assess the maize transcriptomic changes in response to U. maydis. The results revealed differences in hormone signaling, glycometabolism, and photosynthesis after U. maydis infection; specific changes were detected in jasmonic acid (JA), salicylic acid (SA), ethylene (ET), and abscisic acid (ABA) signaling pathways, glycolysis/gluconeogenesis, and photosystems I and II, probably related to defense response. MapMan analysis demonstrated that the differentially expressed genes between the treatment and control groups were clustered into light reaction and photorespiration pathways. In addition, U. maydis inoculation induced chloroplast swelling and damage, suggesting a significant effect on the chloroplast activity and subsequent metabolic process, especially hexose metabolism. A further genetic study using wild-type and galactinol-sucrose galactosyltransferase (gsg) and yellow-green leaf-1 (ygl-1) mutants identified that these two U. maydis-induced genes negatively regulated defense against common smut in maize. Our measurements showed the pathogen early-invasion process, and the key pathways of both chlorophyll biosynthesis and sugar transportation were critical modified in the infected maize line, thereby throwing a light on the molecular mechanisms in the maize-U. maydis interaction.
RESUMEN
Nicosulfuron is a post-emergence herbicide used for weed control in maize fields (Zea mays L.). Here, the pair of nearly isogenic inbred lines SN509-R (nicosulfuron resistant) and SN509-S (nicosulfuron sensitive) was used to study the effect of nicosulfuron on growth, oxidative stress, and the activity and gene expression of antioxidant enzymes in waxy maize seedlings. Nicosulfuron treatment was applied at the five-leaf stage and water treatment was used as control. After nicosulfuron treatment, the death of SN509-S might be associated with increased oxidative stress. Compared with SN509-R, higher O2·- and H2O2 accumulations were observed in SN509-S, which can severely damage lipids and proteins, thus reducing membrane stability. The effects were exacerbated with extended exposure time. Both O2·- and H2O2 detoxification is regulated by enzymes. After nicosulfuron treatment, superoxide dismutase (SOD), catalase, ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), glutathione reductase (GR), and glutathione-S-transferase (GST) of SN509-S were significantly lower than those of SN509-R. Compared to SN509-R, ascorbate content (AA), glutathione (GSH) content, GSH to glutathione disulfide ratios, and AA to dehydroascorbate ratios significantly declined with increasing exposure time in SN509-S. Compared to SN509-S, nicosulfuron treatment increased the transcript levels of most of the APX genes except for APX1, and in contrast to Gst1, upregulated the transcription of sod9, MDHAR, DHAR, and GR genes in SN509-R. These results suggest that on a transcription level and in accordance with their responses, detoxifying enzymes play a vital role in the O2·- and H2O2 detoxification of maize seedlings under nicosulfuron exposure.