Cover illustration: (Top) Seeds of Brassica oleracea DH1012. (Middle) Arabidopsis seeds set at two temperatures. (Bottom) Germinating tomato seeds. Seed quality is a key trait for the vegetable industry where companies can charge high premiums for seed with exceptional performance.
PJ:西南大学揭示植物抗病过程中ABA合成的转录调控机制
Pustule是植物在Xanthomonas citri subsp侵袭诱导的citrus canker disease (CCD)时形成的。9-cis-epoxycarotenoid dioxygenase (NCED)是ABA合成途径的关键酶，过表达会负调控植物对CCD的抗性，过表达株系中 jasmonic acid (JA) 水平显著增高，而salicylic acid (SA)水平显著降低.
过表达CsNCED1-1叶子显著变短，气孔变小，但是密度变大，同时栅栏细胞增多。
前期研究显示CsLOB1和CsbZIP40分别负调控和正调控植物对CCD的抗性。 本研究证实，CsLOB1 和 CsbZIP40 分别直接诱导和抑制CsNCED1-1 的表达，二者竞争性的调控CsNCED1-1 的表达，而 CsbZIP40 表现出更强的对CsNCED1-1 的表达调控能力。
小结：本研究揭示了CsbZIP40和CsLOB1通过调控CsNCED1-1的表达影响植物抗citrus canker disease (CCD)的分子机制。
Hypothetical model of CsNCED1-1 in the development of citrus canker.
Xcc induces the expression of CsLOB1 but not CsbZIP40, leading to increased CsNCED1-1 transcription through CsLOB1 activation. CsNCED1-1 positively regulates ABA accumulation and promotes cell wall degradation and modification as well as proliferation and remodeling of palisade cells, which potentially facilitates pustule formation during pathogen infection. Furthermore, ABA disrupts the crosstalk between JA and SA, thereby suppressing SA-mediated defense mechanisms and ultimately enhancing citrus susceptibility to canker disease. ABA, abscisic acid; JA, jasmonic acid; SA, salicylic acid; Xcc, Xanthomonas citri subsp. citri.
原文：Competitive control of CsNCED1-1 by CsLOB1 and CsbZIP40 triggers susceptibility to citrus canker
