The level of methylesterification alters the functional properties of pectin, which is believed to influence plant growth and development. However, the mechanisms that regulate demethylesterification remain largely unexplored. Pectin with a high degree of methylesterification is produced in the Golgi apparatus and then transferred to the primary cell wall where it is partially demethylesterified by pectin methylesterases (PMEs). Here, we show that in Arabidopsis (Arabidopsis thaliana) seed mucilage, pectin demethylesterification is negatively regulated by the transcription factor ZINC FINGER FAMILY PROTEIN5 (ZAT5). Plants carrying null mutations in ZAT5 had increased PME activity, decreased pectin methylesterification, and produced seeds with a thinner mucilage layer. We provide evidence that ZAT5 binds to a TGATCA-motif and thereby negatively regulates methylesterification by reducing the expression of PME5, HIGHLY METHYL ESTERIFIED SEEDS (HMS)/PME6, PME12, and PME16. We also demonstrate that ZAT5 physically interacts with BEL1-LIKE HOMEODOMAIN2 (BLH2) and BLH4 transcription factors. BLH2 and BLH4 are known to modulate pectin demethylesterification by directly regulating PME58 expression. The ZAT5–BLH2/4 interaction provides a mechanism to control the degree of pectin methylesterification in seed coat mucilage by modifying each transcription factor’s ability to regulate the expression of target genes encoding PMEs. Taken together, these findings reveal a transcriptional regulatory module comprising ZAT5, BLH2 and BLH4, that functions in modulating the de-methylesterification of homogalacturonan in seed coat mucilage.

中文翻译：

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转录因子 ZAT5 和 BLH2/4 调节拟南芥种皮粘液中的同型半乳糖醛酸去甲基酯化


甲基酯化水平改变了果胶的功能特性，这被认为会影响植物的生长和发育。然而，调节去甲基酯化的机制在很大程度上仍未被探索。高度甲基酯化的果胶在高尔基体中产生，然后转移到初生细胞壁，在初生细胞壁中被果胶甲基酯酶 (PME) 部分去甲基酯化。在这里，我们发现在拟南芥 (Arabidopsis thaliana) 种子粘液中，果胶去甲基酯化受到转录因子 ZINC FINGER FAMILY PROTEIN5 (ZAT5) 的负调控。携带 ZAT5 无效突变的植物具有增加的 PME 活性、减少的果胶甲基酯化作用，并产生具有更薄粘液层的种子。我们提供的证据表明，ZAT5 与 TGATCA 基序结合，从而通过降低 PME5、高度甲基酯化种子 (HMS)/PME6、PME12 和 PME16 的表达来负调节甲基酯化。我们还证明 ZAT5 与 BEL1-LIKE HOMEODOMAIN2 (BLH2) 和 BLH4 转录因子发生物理相互作用。已知 BLH2 和 BLH4 通过直接调节 PME58 表达来调节果胶去甲基酯化。 ZAT5-BLH2/4 相互作用提供了一种机制，通过改变每个转录因子调节编码 PME 的靶基因表达的能力来控制种皮粘液中果胶甲基酯化的程度。总而言之，这些发现揭示了一个包含 ZAT5、BLH2 和 BLH4 的转录调控模块，其功能是调节种皮粘液中同型半乳糖醛酸的去甲基酯化。