织物动态平衡,通过居民干细胞的自强和区别完成了,为在整个一个动物的一生的成年纸巾的维护是批评的。成年果蝇肾小体然而,小管(MT 或苍蝇肾) 被肾、肾的干细胞(RNSC ) 经由自我更新的部门维持 RNSC 增长和区别怎么被调整,是不清楚的。这里,我们证明 EGFR/MAPK 发信号为 RNSC 维护是非必需的,但是为 RNSC 增长 invivo 要求。EGFR/MAPK 小径的 Inactivation 堵住或极大地延迟 RNSC 房间周期前进;相反地, EGFR/MAPK 发信号的在激活上导致 RNSC 在增长上并且破坏 renablasts (RB ) 的正常区别, RNSC 部门的立即的女儿。我们的数据进一步建议发信号的 EGFR/MAPK 独立于 JAK/STAT 发信号工作并且 dMyc 和 CycE 部分调停 EGFR/MAPK 在 MT 发信号。一起,我们的数据建议在调整 RNSC 增长发信号的 EGFR/MAPK 的一个主要角色,它可以为理解哺乳动物的肾修理和新生追随者损害提供重要线索。
Tissue homeostasis, accomplished through the self-renewai and differentiation of resident stem cells, is critical for the maintenance of adult tissues throughout an animal's lifetime, Adult Drosophila Malpighian tubules (MTs or fly kidney) are maintained by renal and nephric stem cells (RNSCs) via self-renewing divisions, however, it is unclear how RNSC proliferation and differentiation are regulated. Here we show that EGFR/MAPK signaling is dispensable for RNSC maintenance, but required for RNSC proliferation in vivo. Inacti- vation of the EGFR/MAPK pathway blocks or greatly retards RNSC cell cycle progression; conversely, over-activation of EGFR/MAPK signaling results in RNSC over-proliferation and disrupts the normal differentiation of renablasts (RBs), the immediate daughters of RNSC divisions. Our data further suggest that EGFR/MAPK signaling functions independently of JAK/STAT signaling and that dMyc and CycE partially mediate EGFR/MAPK signaling in MTs. Together, our data suggest a principal role of EGFR/MAPK signaling in regulating RNSC proliferation, which may provide important clues for understanding mammalian kidney repair and regeneration following injury.