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血管祖细胞命运的驱动因素通过抑制肾祖细胞特化来界定中间中胚层的维度。

Drivers of vessel progenitor fate define intermediate mesoderm dimensions by inhibiting kidney progenitor specification.

作者信息

Perens Elliot A, Yelon Deborah

机构信息

Department of Cell and Developmental Biology, School of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA; Department of Pediatrics, Division of Pediatric Nephrology, University of California, San Diego, La Jolla, CA 92093, USA.

Department of Cell and Developmental Biology, School of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.

出版信息

Dev Biol. 2025 Jan;517:126-139. doi: 10.1016/j.ydbio.2024.09.008. Epub 2024 Sep 21.

Abstract

Proper organ formation depends on the precise delineation of organ territories containing defined numbers of progenitor cells. Kidney progenitors reside in bilateral stripes of posterior mesoderm that are referred to as the intermediate mesoderm (IM). Previously, we showed that the transcription factors Hand2 and Osr1 act to strike a balance between the specification of the kidney progenitors in the IM and the vessel progenitors in the laterally adjacent territory. Recently, the transcription factor Npas4l - an early and essential driver of vessel and blood progenitor formation - was shown to inhibit kidney development. Here we demonstrate how kidney progenitor specification is coordinated by hand2, osr1, and npas4l. We find that npas4l and the IM marker pax2a are transiently co-expressed in the posterior lateral mesoderm, and npas4l is necessary to inhibit IM formation. Consistent with the expression of npas4l flanking the medial and lateral sides of the IM, our findings suggest roles for npas4l in defining the IM boundaries at each of these borders. At the lateral IM border, hand2 promotes and osr1 inhibits the formation of npas4l-expressing lateral vessel progenitors, and hand2 requires npas4l to inhibit IM formation and to promote vessel formation. Meanwhile, npas4l appears to have an additional role in suppressing IM fate at the medial border: npas4l loss-of-function enhances hand2 mutant IM defects and results in excess IM generated outside of the lateral hand2-expressing territory. Together, our findings reveal that establishment of the medial and lateral boundaries of the IM requires inhibition of kidney progenitor specification by the neighboring drivers of vessel progenitor fate.

摘要

正常的器官形成依赖于对含有特定数量祖细胞的器官区域进行精确划分。肾祖细胞位于后中胚层的双侧条带中,该区域被称为中间中胚层(IM)。此前,我们发现转录因子Hand2和Osr1在IM中肾祖细胞与相邻外侧区域血管祖细胞的特化之间起到平衡作用。最近,转录因子Npas4l(血管和血液祖细胞形成的早期关键驱动因子)被证明会抑制肾脏发育。在此,我们展示了Hand2、Osr1和Npas4l如何协调肾祖细胞的特化。我们发现Npas4l与IM标记物Pax2a在后外侧中胚层中短暂共表达,且Npas4l对于抑制IM形成是必需的。与Npas4l在IM内侧和外侧两侧的表达情况一致,我们的研究结果表明Npas4l在界定这些边界处的IM边界方面发挥作用。在IM外侧边界,Hand2促进而Osr1抑制表达Npas4l的外侧血管祖细胞的形成,且Hand2需要Npas4l来抑制IM形成并促进血管形成。同时,Npas4l在内侧边界似乎还有抑制IM命运的额外作用:Npas4l功能丧失会增强Hand2突变体的IM缺陷,并导致在外侧Hand2表达区域之外产生过多的IM。总之,我们的研究结果表明,IM内侧和外侧边界的建立需要通过相邻的血管祖细胞命运驱动因子抑制肾祖细胞特化。

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