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ARS Home » Midwest Area » Ames, Iowa » Corn Insects and Crop Genetics Research » Research » Publications at this Location » Publication #294586
Title: Replication protein A subunit 3 and the iron efficiency response in soybean

Author
item ATWOOD, SARAH - Iowa State University
item O'ROURKE, JAMIE - Iowa State University
item PEIFFER, GREGORY - Iowa State University
item YIN, TENGFEI - Iowa State University
item MAJUMDER, MAHBUBUL - Iowa State University
item ZHANG, CHUNQUAN - Iowa State University
item CIANZIO, SILVIA - Iowa State University
item HILL, JOHN - Iowa State University
item COOK, DIANNE - Iowa State University
item WHITHAM, STEVEN - Iowa State University
item Shoemaker, Randy
item Graham, Michelle

Submitted to: Plant Cell and Environment
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/28/2013
Publication Date: 6/1/2013
Citation: Atwood, S., O'Rourke, J.A., Peiffer, G., Yin, T., Majumder, M., Zhang, C., Cianzio, S., Hill, J., Cook, D., Whitham, S., Shoemaker, R.C., Graham, M.A. 2013. Replication protein A subunit 3 and the iron efficiency response in soybean. Plant Cell and Environment. DOI: 10.1111/pce.12147.

Interpretive Summary: Iron is a micronutrient required for proper growth and development of plants. Iron deficiency results in stunting and yield losses. Understanding how plants respond to iron stress is critical to ensuring a steady soybean yield. Recent experiments have suggested that plants resistant to iron deficiency chlorosis (IDC) regulate the activity of iron acquisition, stress tolerance and DNA replication genes. To understand the role DNA replication plays in IDC, we examined a family of genes involved in DNA replication in soybean lines resistant or susceptible to iron deficiency. We found that iron deficiency resistant lines turn off DNA replication genes during iron stress while iron deficiency susceptible lines turned on DNA replication genes. We then turned off a core DNA replication gene in the iron deficiency susceptible line to see if this resulted in greater tolerance to iron stress. Once the DNA replication machinery was turned off, normally iron deficient susceptible lines were greener and showed fewer IDC symptoms. By measuring the activity of all genes in these plants, we found the turning off DNA replication activated genes involved defense, stress, iron uptake and nutrient acquisition but repressed genes involved in growth, photosynthesis and protein production. Slowing growth in response to nutrient deficiency may explain why iron efficient soybean lines tend to have lower yields. This information provides one more target for improving soybean yield in areas where IDC is a problem.

Technical Abstract: In soybean [Glycine max (L.) Merr.], iron deficiency results in interveinal chlorosis and decreased photosynthetic capacity, leading to stunting and yield loss. In this study, gene expression analyses investigated the role of soybean replication protein A (RPA) subunits during iron stress. Nine RPA homologs were significantly differentially expressed in response to iron stress in the near isogenic lines (NILs) Clark (iron efficient) and Isoclark (iron inefficient). RPA homologs exhibited opposing expression patterns in the two NILs, with RPA expression significantly repressed during iron deficiency in Clark but induced in Isoclark. We used virus induced gene silencing (VIGS) to repress GmRPA3 expression in the iron inefficient line Isoclark and mirror expression in Clark. GmRPA3-silenced plants had improved IDC symptoms and chlorophyll content under iron deficient conditions and also displayed stunted growth regardless of iron availability. RNA-Seq comparing gene expression between GmRPA3-silenced and empty vector plants revealed massive transcriptional reprogramming with differential expression of genes associated with defense, immunity, aging, death, protein modification, protein synthesis, photosynthesis and iron uptake and transport genes. Our findings suggest the iron efficient genotype Clark is able to induce energy controlling pathways, possibly regulated by SnRK1/TOR, to promote nutrient recycling and stress responses in iron deficient conditions.