Department of Plant Biology and Ecology, College of Life Sciences, Nankai University and Tianjin Key Laboratory of Protein Sciences, 300071, Tianjin, China.
Department of Plant Sciences, MIGAL-Galilee Research Institute, Kiryat-Shmona 11016, Israel.
Plant Physiol. 2021 Jun 11;186(2):1101-1121. doi: 10.1093/plphys/kiab138.
In Arabidopsis thaliana, mitochondrial-localized heat-shock cognate protein 70-1 (mtHSC70-1) plays an important role in vegetativegrowth. However, whether mtHSC70-1 affects reproductive growth remains unknown. Here, we found that the mtHSC70-1 gene was expressed in the provascular cells of the embryo proper from the early heart stage onward during embryogenesis. Phenotypic analyses of mthsc70-1 mutants revealed that mtHSC70 deficiency leads to defective embryo development and that this effect is mediated by auxin. In addition to a dwarf phenotype, the mthsc70-1 mutant displayed defects in flower morphology, anther development, and embryogenesis. At early developmental stages, the mthsc70-1 embryos exhibited abnormal cell divisions in both embryo proper and suspensor cells. From heart stage onward, they displayed an abnormal shape such as with no or very small cotyledon protrusions, had aberrant number of cotyledons, or were twisted. These embryo defects were associated with reduced or ectopic expression of auxin responsive reporter DR5rev:GFP. Consistently, the expression of auxin biosynthesis and polar auxin transport genes were markedly altered in mthsc70-1. On the other hand, mitochondrial retrograde regulation (MRR) was enhanced in mthsc70-1. Treatment of wild-type plants with an inhibitor that activates mitochondrial retrograde signaling reduced the expression level of auxin biosynthesis and polar auxin transport genes and induced phenotypes similar to those of mthsc70-1. Taken together, our data reveal that loss of function of mtHSC70-1 induces MRR, which inhibits auxin biosynthesis and polar auxin transport, leading to abnormal auxin gradients and defective embryo development.
在拟南芥中，线粒体定位的热休克同源蛋白 70-1（mtHSC70-1）在营养生长中发挥重要作用。然而，mtHSC70-1 是否影响生殖生长尚不清楚。在这里，我们发现 mtHSC70-1 基因在胚胎发生过程中从早期心脏阶段开始就在胚胎的原血管细胞中表达。mthsc70-1 突变体的表型分析表明，mtHSC70 缺乏导致胚胎发育缺陷，这种影响是由生长素介导的。除了矮化表型外，mthsc70-1 突变体还表现出花形态、花药发育和胚胎发生缺陷。在早期发育阶段，mthsc70-1 胚胎在原胚和悬浮细胞中表现出异常的细胞分裂。从心脏阶段开始，它们表现出异常的形状，例如没有或只有很小的子叶突起、子叶数量异常或扭曲。这些胚胎缺陷与生长素响应报告基因 DR5rev:GFP 的表达减少或异位表达有关。一致地，mthsc70-1 中生长素生物合成和极性生长素运输基因的表达明显改变。另一方面，mthsc70-1 中增强了线粒体逆行调节（MRR）。用激活线粒体逆行信号的抑制剂处理野生型植物会降低生长素生物合成和极性生长素运输基因的表达水平，并诱导出与 mthsc70-1 相似的表型。总之，我们的数据表明，mtHSC70-1 功能丧失会诱导 MRR，从而抑制生长素的生物合成和极性运输，导致异常的生长素梯度和胚胎发育缺陷。
