Skip to main content
ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Sunflower and Plant Biology Research » Research » Publications at this Location » Publication #277066

Title: Microarray and growth analyses identify differences and similarities of early corn response to weeds, shade, and nitrogen stress

Author
item MORILES, JANET - South Dakota State University
item HANSEN, STEPHANIE - South Dakota State University
item Horvath, David
item REICKS, GRAIG - South Dakota State University
item CLAY, DAVID - South Dakota State University
item CLAY, SHARON - South Dakota State University

Submitted to: Weed Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/8/2011
Publication Date: 4/1/2012
Citation: Moriles, J., Hansen, S., Horvath, D.P., Reicks, G., Clay, D.E., Clay, S.A. 2012. Microarray and growth analyses identify differences and similarities of early corn response to weeds, shade, and nitrogen stress. Weed Science. 60(2):158-166.

Interpretive Summary: Weeds reduce crop yields, and it was always assumed that this was because weeds compete with crops for nutrients, water and light. However, recent experiments suggest that weeds might reduce crop yields through other mechanisms. This work compared the changes in growth, morphology, yield and gene expression that occur when corn is grown either in the presence of weeds, or when it is stressed by shade or by low nitrogen levels under conditions where water was not limiting. Some similarities between the various stresses were observed. However, the large numbers of differences in the genes that are turned on or off, and in the development and growth of the corn that was grown in the presence of weeds strongly suggests that direct competition for light or nitrogen are not sufficient to explain the reduction in growth and yield caused by weeds. Thus, weed stress appears to reduce crop yield by mechanisms other than direct competition for resources.

Technical Abstract: Weed interference with crop growth is often attributed to water, nutrient, or light competition; however, specific physiological responses to these stresses are not well described. This study’s objective was to compare growth, yield, and gene expression responses of corn to nitrogen (N), low light (40% shade), and weed stresses. Corn vegetative parameters from V2 to V12 stages, yield parameters, and gene expression using transcriptome (2008) and quantitative polymerase chain reaction (qPCR) (2008/09) analyses at V8 were compared among the stresses and with nonstressed corn. N stress did not affect vegetative parameters, although grain yield was reduced by 40% compared with nonstressed plants. Shade, present until V2, reduced biomass and leaf area >50% at V2, and recovering plants remained smaller than nonstressed plants at V12. However, grain yields of shade-stressed and nonstressed plants were similar, unless shade remained until V8. Weed stress reduced corn growth and yield in 2008 when weeds remained until V6. In 2009, weed stress until V2 reduced corn vegetative growth, but yield reductions occurred only if weed stress remained until V6 or later. Principle component analysis of differentially expressed genes indicated that shade and weed stress had more similar gene expression patterns to each other than they did to nonstressed or N-stressed tissues. However, corn grown in N-stressed conditions shared 252 differentially expressed genes with weed-stressed plants. Ontologies associated with light/photosynthesis, energy conversion, and signaling were down-regulated in response to all three stresses. Shade and weed stress clustered most tightly together, based on gene expression, but shared only three ontologies, O-METHYLTRANSFERASE activity (lignification processes), POLY(U)-BINDING activity (posttranscriptional gene regulation), and stomatal movement. Based on morphologic and genomic observations, weed stress to corn was not explained by individual effects of N or light stress. Therefore, we hypothesize that these stresses share limited signaling mechanisms.