Suppression of CsFAD3 in a JA-dependent manner but not the SA pathway impaired drought stress tolerance in tea1

The growth and yield of tea plants are seriously limited by drought stress. Fatty acid desaturations (FADs) contribute to mediating membrane fluidity in response to different stresses; however, the role of ω-3 FAD (Omega-3 fatty acid desaturase)-mediated damage induced by drought stress in tea plants is poorly understood. In this study, drought stress significantly promoted the synthesis of C18:3 (linolenic acid) and the expression level of CsFAD3. Yeast experiments further demonstrated that CsFAD3 can convert C18:2 to C18:3 and that the 35S:GFP-CsFAD3 fusion protein was localized in the endoplasmic reticulum of Nicotiana benthamiana (N. benthamiana) cells. CsFAD3-silenced tea leaves exhibited poor drought tolerance, with lower Fv/Fm and greater MDA (malondialdehyde) content compared with those of control plants. However, transgenic 35S:CsFAD3 Arabidopsis plants showed opposite phenotypes. In addition, JA (jasmonic acid) contents and the expression levels of CsLOX2, CsLOX4, CsAOS, CsAOC3 and CsOPR were significantly reduced in CsFAD3-silenced leaves under drought stress. However, no substantial difference in SA (salicylic acid) content was detected under normal or drought conditions. Analysis of Atcoi1 (JA receptor) or Atnpr1 (SA receptor) mutant Arabidopsis plants in 35S:CsFAD3 backgrounds further revealed that knockout of Atcoi1 impaired the drought-tolerant phenotypes of CsFAD3 overexpression lines. Therefore, our study demonstrated that CsFAD3 played a crucial role in drought tolerance by mediating JA pathways.