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Eater 与 Multiplexin 合作驱动造血隔室的形成。

Eater cooperates with Multiplexin to drive the formation of hematopoietic compartments.

机构信息

Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.

Molecular Cell Biology, Institute I for Anatomy, University of Cologne Medical School, Cologne, Germany.

出版信息

Elife. 2020 Oct 7;9:e57297. doi: 10.7554/eLife.57297.

DOI:10.7554/eLife.57297
PMID:33026342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7541089/
Abstract

Blood development in multicellular organisms relies on specific tissue microenvironments that nurture hematopoietic precursors and promote their self-renewal, proliferation, and differentiation. The mechanisms driving blood cell homing and their interactions with hematopoietic microenvironments remain poorly understood. Here, we use the model to reveal a pivotal role for basement membrane composition in the formation of hematopoietic compartments. We demonstrate that by modulating extracellular matrix components, the fly blood cells known as hemocytes can be relocated to tissue surfaces where they function similarly to their natural hematopoietic environment. We establish that the Collagen XV/XVIII ortholog Multiplexin in the tissue-basement membranes and the phagocytosis receptor Eater on the hemocytes physically interact and are necessary and sufficient to induce immune cell-tissue association. These results highlight the cooperation of Multiplexin and Eater as an integral part of a homing mechanism that specifies and maintains hematopoietic sites in .

摘要

多细胞生物的血液发育依赖于特定的组织微环境,这些微环境滋养造血前体并促进其自我更新、增殖和分化。驱动血细胞归巢的机制及其与造血微环境的相互作用仍知之甚少。在这里,我们使用 模型揭示了基底膜组成在造血隔室形成中的关键作用。我们证明,通过调节细胞外基质成分,被称为血细胞的果蝇血液细胞可以被重新定位到组织表面,在那里它们的功能类似于其自然造血环境。我们确定组织基底膜中的胶原 XV/XVIII 同源物 Multiplexin 和血细胞上的吞噬受体 Eater 相互物理作用,并且是诱导免疫细胞与组织结合所必需且充分的。这些结果强调了 Multiplexin 和 Eater 的合作是一个归巢机制的组成部分,该机制指定并维持 中的造血部位。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/e97dcda7ce7e/elife-57297-resp-fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/e97dcda7ce7e/elife-57297-resp-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/8f75045d04c1/elife-57297-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/a8b378e617f3/elife-57297-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/74e9b7b554a0/elife-57297-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/e81f267d6f6c/elife-57297-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/286416379ab6/elife-57297-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/49f4209eded1/elife-57297-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/c244328eeeda/elife-57297-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/e84316548192/elife-57297-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/d9600f1cb1bf/elife-57297-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/e9ae147e20a9/elife-57297-fig5-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/433cdf292eeb/elife-57297-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/4451b2eed3e4/elife-57297-fig6-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/773a/7541089/e97dcda7ce7e/elife-57297-resp-fig1.jpg

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