Suppression of CsFAD3 in a JA-dependent manner, but not through the SA pathway, impairs drought stress tolerance in tea

Abstract

The growth and yield of tea plants are seriously limited by drought stress. Fatty acid desaturases (FADs) contribute to the mediation of membrane fluidity in response to different stresses, although 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 cells. CsFAD3-silenced tea leaves exhibited poor drought tolerance, with a lower Fv/Fm and a higher malondialdehyde (MDA) content than the control plants. However, transgenic 35S:CsFAD3 Arabidopsis plants showed the opposite phenotypes. In addition, the jasmonic acid (JA) content and the expression levels of CsLOX2, CsLOX4, CsAOS, CsAOC3 and CsOPR2 were significantly reduced in CsFAD3-silenced leaves under drought stress. However, no substantial difference in the salicylic acid (SA) content was detected under normal or drought conditions. An 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, this study demonstrated that CsFAD3 plays a crucial role in drought tolerance by mediating JA pathways.