The Golgi apparatus is an organelle where membrane or secretory proteins receive post-translational modifications such as glycosylation and sulfation, after which the proteins are selectively transported to their final destinations through vesicular transport. When the synthesis of secretory or membrane proteins is increased and overwhelms the capacity of the Golgi (Golgi stress), eukaryotic cells activate a homeostatic mechanism called the Golgi stress response to augment the capacity of the Golgi. Four response pathways of the Golgi stress response have been identified, namely the TFE3, CREB3, HSP47, and proteoglycan pathways, which regulate the general function of the Golgi, apoptosis, cell survival, and proteoglycan glycosylation, respectively. Here, we identified a novel response pathway that augments the expression of glycosylation enzymes for mucins in response to insufficiency in mucin-type glycosylation in the Golgi (mucin-type Golgi stress), and we found that expression of glycosylation enzymes for mucins such as GALNT5, GALNT8, and GALNT18 was increased upon mucin-type-Golgi stress. We named this pathway the mucin pathway. Unexpectedly, mucin-type Golgi stress induced the expression and activation of TFE3, a key transcription factor regulating the TFE3 pathway, suggesting that the activated mucin pathway sends a crosstalk signal to the TFE3 pathway. We identified an enhancer element regulating transcriptional induction of TFE3 upon mucin-type Golgi stress, and named it the mucin-type Golgi stress response element, of which consensus was ACTTCC(N9)TCCCCA. These results suggested that crosstalk from the mucin pathway to the TFE3 pathway has an important role in the regulation of the mammalian Golgi stress response.Key words: Golgi stress, mucin, TFE3, organelle autoregulation, organelle zone.

中文翻译：

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MGSE调节从粘蛋白途径到高尔基体应激反应的TFE3途径的串扰。

高尔基体是一种细胞器，细胞膜或分泌蛋白接受翻译后修饰，例如糖基化和硫酸化，然后通过水泡运输将蛋白选择性地运输到其最终目的地。当分泌蛋白或膜蛋白的合成增加并压倒了高尔基体的能力（高尔基体应激）时，真核细胞会激活一种称为高尔基体应激反应的稳态机制，以增强高尔基体的能力。已经确定了高尔基体应激反应的四个反应途径，即TFE3，CREB3，HSP47和蛋白聚糖途径，它们分别调节了高尔基体的一般功能，凋亡，细胞存活和蛋白聚糖糖基化。这里，我们发现了一种新的应答途径，该应答途径可响应高尔基体中粘蛋白型糖基化不足（粘蛋白型高尔基体应激）而增加粘蛋白糖基化酶的表达，并且我们发现粘蛋白如GALNT5，GALNT8的糖基化酶表达，并且在粘蛋白型高尔基体应激时GALNT18升高。我们将该途径称为粘蛋白途径。出乎意料的是，粘蛋白型高尔基体应激诱导TFE3的表达和激活，TFE3是调节TFE3途径的关键转录因子，提示激活的粘蛋白途径向TFE3途径发送了串扰信号。我们鉴定了一种在粘蛋白型高尔基体应激后调节TFE3转录诱导的增强子元件，并将其命名为粘蛋白型高尔基体应激反应元件，其共识是ACTTCC（N9）TCCCCA。