In Drosophila, the replacement of spent enterocytes (ECs) relies on division of intestinal stem cells (ISCs) and differentiation of their progeny, the enteroblasts (EBs). Recent studies have revealed a role for JAK/STAT signaling in the modulation of the rate of ISC division in response to environmental challenge. Here, we demonstrate the critical role of the UPD3 cytokine in the JAK/STAT-dependent response to enteric infection. We show that upd3 expression is activated in ECs and in EBs that massively differentiate in response to challenge. We show that the UPD3 cytokine, which is secreted basally and accumulates at the basement membrane, is required for stimulation of JAK/STAT signaling in EBs and visceral muscles (VMs). We further show that stimulation of ISC division requires active JAK/STAT signaling in EBs and VMs, but apparently not in ISCs. Our results suggest that EBs and VMs modulate the rate of the EGFR-dependent ISC division through upd3-dependent production of the EGF ligands Spitz and Vein, respectively. This study therefore supports the notion that the production of the UPD3 cytokine in stem cell progeny (ECs and EBs) stimulates intestinal stem cell division through modulation of JAK/STAT signaling in the stem cell microenvironment (EBs and VMs).

译文

在果蝇中,用过的肠细胞 (ECs) 的替代依赖于肠干细胞 (isc) 的分裂及其后代,肠成细胞 (EBs) 的分化。最近的研究表明,JAK/STAT信号在响应环境挑战的ISC划分速率调节中的作用。在这里,我们证明了UPD3细胞因子在JAK/STAT依赖性肠道感染反应中的关键作用。我们证明了upd3表达在ECs和EBs中被激活,这些响应挑战而发生了巨大分化。我们表明,UPD3细胞因子是基底分泌并积聚在基底膜上的,是刺激EBs和内脏肌肉 (VMs) 中JAK/STAT信号传导所必需的。我们进一步表明,刺激ISC分区需要在EBs和vm中发出主动的JAK/STAT信号,但显然不在ISC中。我们的结果表明,EBs和VMs分别通过upd3-dependent产生EGF配体Spitz和静脉来调节EGFR依赖性ISC分裂的速率。因此,这项研究支持以下观点: 干细胞后代 (ECs和EBs) 中UPD3细胞因子的产生通过调节干细胞微环境 (EBs和VMs) 中的JAK/STAT信号来刺激肠道干细胞分裂。

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