Role for compartmentalization in nephron progenitor differentiation

被引：110

作者：

Brown, Aaron C. ^{[1
]}

Muthukrishnan, Deepthi ^{[1
]}

Guay, Justin A. ^{[1
]}

Adams, Derek C. ^{[1
]}

Schafer, Dillon A. ^{[1
]}

Fetting, Jennifer L. ^{[1
]}

Oxburgh, Leif ^{[1
]}

机构：

[1] Maine Med Ctr, Res Inst, Ctr Mol Med, Scarborough, ME 04074 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2013年 / 110卷 / 12期

关键词：

cap mesenchyme; niche; pretubular aggregate; nephrogenic zone; kidney development; MOUSE METANEPHROGENIC MESENCHYME; KIDNEY DEVELOPMENT; MAMMALIAN KIDNEY; POPULATION; INDUCTION; RENEWAL; SIX2; NEPHROGENESIS; DEFINES; MICE;

D O I：

10.1073/pnas.1213971110

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Embryonic nephron progenitor cells are segregated in molecularly distinct compartments of unknown function. Our study reveals an integral role for bone morphogenetic protein-SMAD in promoting transition of progenitors from the primitive Cbp/p300-interacting transactivator 1 expressing (CITED1+) compartment to the uniquely sine oculis-related homeobox 2 expressing (SIX2-only) compartment where they become inducible by wingless-type mouse mammary tumor virus integration site family member (WNT)/beta-catenin signaling. Significantly, CITED1(+) cells are refractory to WNT/beta-catenin induction. We propose a model in which the primitive CITED1(+) compartment is refractory to induction by WNT9b/beta-catenin, ensuring maintenance of undifferentiated progenitor cells for future nephrogenesis. Bone morphogenetic protein 7-SMAD is then required for transition to a distinct compartment in which cells become inducible by WNT9b/beta-catenin, allowing them to progress toward epithelialization.

引用

页码：4640 / 4645

页数：6

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