Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size.
Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size.
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DOI：
10.7554/elife.64125
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发表时间：
2021-09-23
期刊：
影响因子：
7.7
通讯作者：
Buchon N
中科院分区：
文献类型：
--
作者：
Bonfini A;Dobson AJ;Duneau D;Revah J;Liu X;Houtz P;Buchon N
肠道是动物和食物之间的主要界面，但它如何适应定性饮食变化的定义很差。我们发现，果蝇中肠可塑性调整后，饮食组成的变化。一组营养素共同促进肠道生长，而糖则相反。饮食影响肠上皮细胞损失和干细胞增殖的绝对和相对水平，它们共同决定细胞数量。饮食也影响肠上皮细胞的大小。高糖饮食抑制翻译并使肠道干细胞增殖与小生境来源信号的表达脱钩，但令人惊讶的是，从遗传上挽救这些效应并不足以改变饮食对中肠大小的影响。然而，当干细胞增殖不足时，饮食对肠上皮细胞大小的影响增强，减少肠上皮细胞自主TOR信号足以减弱饮食依赖性中肠蠕动。这些数据阐明了营养、上皮动力学和细胞大小之间的复杂关系，并揭示了一种新的可塑性、饮食依赖性器官再生模式。
The gut is the primary interface between an animal and food, but how it adapts to qualitative dietary variation is poorly defined. We find that the Drosophila midgut plastically resizes following changes in dietary composition. A panel of nutrients collectively promote gut growth, which sugar opposes. Diet influences absolute and relative levels of enterocyte loss and stem cell proliferation, which together determine cell numbers. Diet also influences enterocyte size. A high sugar diet inhibits translation and uncouples intestinal stem cell proliferation from expression of niche-derived signals, but, surprisingly, rescuing these effects genetically was not sufficient to modify diet’s impact on midgut size. However, when stem cell proliferation was deficient, diet’s impact on enterocyte size was enhanced, and reducing enterocyte-autonomous TOR signaling was sufficient to attenuate diet-dependent midgut resizing. These data clarify the complex relationships between nutrition, epithelial dynamics, and cell size, and reveal a new mode of plastic, diet-dependent organ resizing.