WIND1-based acquisition of regeneration competency in Arabidopsis and rapeseed

• DOI: 10.1007/s10265-015-0714-y
• Publication Date: 2015-03-25T14:46:46Z
• Authors: Akira Iwase; Kento Mita; Satoko Nonaka; Momoko Ikeuchi; Chie Koizuka; Mariko Ohnuma; Hiroshi Ezura; Jun Imamura; Keiko Sugimoto
• Keywords: Plant Somatic Embryogenesis Techniques; 0303 health sciences; Indoleacetic Acids; Arabidopsis Proteins; Brassica napus; Arabidopsis; Plants, Genetically Modified; Plant Roots; Plant Leaves; 03 medical and health sciences; Plant Growth Regulators; Organ Specificity; Regeneration; Plant Shoots; Plant Proteins; Transcription Factors

Callus formation and de novo organogenesis often occur in the wounded tissues of plants. Although this regenerative capacity of plant cells has been utilized for many years, molecular basis for the wound-induced acquisition of regeneration competency is yet to be elucidated. Here we find that wounding treatment is essential for shoot regeneration from roots in the conventional tissue culture of Arabidopsis thaliana. Furthermore, we show that an AP2/ERF transcription factor WOUND INDUCED DEDIFFERENTIATION1 (WIND1) plays a pivotal role for the acquisition of regeneration competency in the culture system. Ectopic expression of WIND1 can bypass both wounding and auxin pre-treatment and increase de novo shoot regeneration from root explants cultured on shoot-regeneration promoting media. In Brassica napus, activation of Arabidopsis WIND1 also greatly enhances de novo shoot regeneration, further corroborating the role of WIND1 in conferring cellular regenerative capacity. Our data also show that sequential activation of WIND1 and an embryonic regulator LEAFY COTYLEDON2 enhances generation of embryonic callus, suggesting that combining WIND1 with other transcription factors promote efficient and organ-specific regeneration. Our findings in the model plant and crop plant point to a possible way to efficiently induce callus formation and regeneration by utilizing transcription factors as a molecular switch.