Location: Plant Science ResearchTitle: Genetic and physiological characterization of a Calcium deficiency phenotype in maize
|WANG, YANLI - North Carolina State University|
|MARTINS, LAIS - North Carolina State University|
Submitted to: G3, Genes/Genomes/Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/1/2020
Publication Date: 4/1/2020
Citation: Wang, Y., Martins, L., Sermons, S.M., Balint Kurti, P.J. 2020. Genetic and physiological characterization of a Calcium deficiency phenotype in maize. G3, Genes/Genomes/Genetics. https://doi.org/10.1534/g3.120.401069.
Interpretive Summary: We have identified a leaf necrosis trait caused by over-fertilization of certain maize lines. We have shown that it as caused by a deficiency of calcium and have mapped genes that provide some resistance to these necrosis symptoms.
Technical Abstract: Calcium (Ca) is an essential plant nutrient. It is required for signaling, cell wall fortification and plays an important role in maize growth and development. Calcium deficiency (Ca-deficiency) in maize causes leaf tip rot and a so-called “buggy-whipping” phenotype. Seedlings of the maize line B73 displayed these Ca-deficiency symptoms when grown in the greenhouse with excess fertilizer during the winter months. Seedlings of the Mo17 maize line did not display these symptoms under the same conditions. These differential phenotypes could be recapitulated in ‘mini-hydroponic’ systems in the laboratory in which high ammonium, but not nitrate, levels induced the symptoms in B73 seedlings and addition of Ca2+ ameliorated them. Furthermore, elemental analysis showed that the Ca content in B73 seedling leaves was reduced when grown under high fertilizer conditions. These data suggest strongly that ammonium reduces the seedling’s ability to absorb calcium, which causes the Ca-deficiency phenotype, and this trait varies among genotypes. A recombinant inbred line (RIL) population derived from a B73 x Mo17 cross was used to map quantitative trait loci (QTL) associated with the Ca deficiency phenotype. QTL associated with variation in susceptibility to Ca deficiency were detected on chromosomes 1, 2, 3 and 6 which explained between 3.30%-9.94% of the observed variation. Several genes predicted to bind or be activated by calcium map to the strongest of these QTL on chromosome 2. These results describe for the first time the genetics of Ca-deficiency symptoms in maize and in plants in general.