a State Key Laboratory of Biocontrol, Guangdong Provincial Key Laboratory of Plant Resources, School of Life Sciences , Sun Yat-sen University , Guangzhou , China.
Autophagy. 2019 Mar;15(3):407-422. doi: 10.1080/15548627.2018.1520547. Epub 2018 Sep 22.
Glucose produced from photosynthesis is a key nutrient signal regulating root meristem activity in plants; however, the underlying mechanisms remain poorly understood. Here, we show that, by modulating reactive oxygen species (ROS) levels, the conserved macroautophagy/autophagy degradation pathway contributes to glucose-regulated root meristem maintenance. In Arabidopsis thaliana roots, a short exposure to elevated glucose temporarily suppresses constitutive autophagosome formation. The autophagy-defective autophagy-related gene (atg) mutants have enhanced tolerance to glucose, established downstream of the glucose sensors, and accumulate less glucose-induced ROS in the root tips. Moreover, the enhanced root meristem activities in the atg mutants are associated with improved auxin gradients and auxin responses. By acting with AT4G39850/ABCD1 (ATP-binding cassette D1; Formerly PXA1/peroxisomal ABC transporter 1), autophagy plays an indispensable role in the glucose-promoted degradation of root peroxisomes, and the atg mutant phenotype is partially rescued by the overexpression of ABCD1. Together, our findings suggest that autophagy is an essential mechanism for glucose-mediated maintenance of the root meristem. Abbreviation: ABA: abscisic acid; ABCD1: ATP-binding cassette D1; ABO: ABA overly sensitive; AsA: ascorbic acid; ATG: autophagy related; CFP: cyan fluorescent protein; Co-IP: co-immunoprecipitation; DAB: 3',3'-diaininobenzidine; DCFH-DA: 2',7'-dichlorodihydrofluorescin diacetate; DR5: a synthetic auxin response element consists of tandem direct repeats of 11 bp that included the auxin-responsive TGTCTC element; DZ: differentiation zone; EZ, elongation zone; GFP, green fluorescent protein; GSH, glutathione; GUS: β-glucuronidase; HXK1: hexokinase 1; HO: hydrogen peroxide; IAA: indole-3-acetic acid; IBA: indole-3-butyric acid; KIN10/11: SNF1 kinase homolog 10/11; MDC: monodansylcadaverine; MS: Murashige and Skoog; MZ: meristem zone; NBT: nitroblue tetrazolium; NPA: 1-N-naphtylphthalamic acid; OxIAA: 2-oxindole-3-acetic acid; PIN: PIN-FORMED; PLT: PLETHORA; QC: quiescent center; RGS1: Regulator of G-protein signaling 1; ROS: reactive oxygen species; SCR: SCARECROW; SHR, SHORT-ROOT; SKL: Ser-Lys-Leu; SnRK1: SNF1-related kinase 1; TOR: target of rapamycin; UPB1: UPBEAT1; WOX5: WUSCHEL related homeobox 5; Y2H: yeast two-hybrid; YFP: yellow fluorescent protein.
光合作用产生的葡萄糖是调节植物根分生组织活性的关键营养信号；然而，其潜在机制仍知之甚少。在这里，我们表明，通过调节活性氧（ROS）水平，保守的巨自噬/自噬降解途径有助于葡萄糖调节的根分生组织维持。在拟南芥根中，短暂暴露于高浓度葡萄糖会暂时抑制组成型自噬体的形成。自噬缺陷型自噬相关基因（atg）突变体对葡萄糖的耐受性增强，位于葡萄糖传感器的下游，并在根尖积累较少的葡萄糖诱导的 ROS。此外，atg 突变体中增强的根分生组织活性与改善的生长素梯度和生长素反应有关。通过与 AT4G39850/ABCD1（ATP 结合盒 D1；以前的 PXA1/过氧化物酶体 ABC 转运蛋白 1）合作，自噬在葡萄糖促进的根过氧化物酶体降解中发挥不可或缺的作用，atg 突变体表型部分通过 ABCD1 的过表达得到挽救。总之，我们的研究结果表明，自噬是葡萄糖介导的根分生组织维持的必要机制。缩写：ABA：脱落酸；ABCD1：ATP 结合盒 D1；ABO：ABA 过度敏感；AsA：抗坏血酸；ATG：自噬相关；CFP：青色荧光蛋白；Co-IP：免疫共沉淀；DAB：3',3'-二氨基联苯胺；DCFH-DA：2',7'-二氯二氢荧光素二乙酸酯；DR5：由串联重复 11 个碱基的串联直接重复组成的合成生长素反应元件，包括生长素反应 TGTCTC 元件；DZ：分化区；EZ，伸长区；GFP，绿色荧光蛋白；GSH，谷胱甘肽；GUS：β-葡萄糖醛酸酶；HXK1：己糖激酶 1；HO：过氧化氢；IAA：吲哚-3-乙酸；IBA：吲哚-3-丁酸；KIN10/11：SNF1 激酶同源物 10/11；MDC：单丹磺酰尸胺；MS：Murashige 和 Skoog；MZ：分生组织区；NBT：硝基蓝四唑；NPA：1-N-萘基邻氨甲酰苯甲酸；OxIAA：2-氧吲哚-3-乙酸；PIN：PIN 形成；PLT：PLETHORA；QC：静止中心；RGS1：G 蛋白信号调节因子 1；ROS：活性氧；SCR：SCARECROW；SHR，SHORT-ROOT；SKL：Ser-Lys-Leu；SnRK1：SNF1 相关激酶 1；TOR：雷帕霉素的靶点；UPB1：UPBEAT1；WOX5：WUSCHEL 相关同源框 5；Y2H：酵母双杂交；YFP：黄色荧光蛋白。
