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Generation of a T lx1 C re ER ‐ V enus knock‐in mouse strain for the study of spleen development
Author(s) -
Nakahara Ryo,
Kawai Yasuhiro,
Oda Akihisa,
Nishimura Miyuki,
Murakami Akikazu,
Azuma Takachika,
Kaifu Tomonori,
Goitsuka Ryo
Publication year - 2014
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.22829
Subject(s) - spleen , microbiology and biotechnology , biology , stromal cell , mesenchymal stem cell , cancer research , immunology
Summary The spleen is a lymphoid organ that serves as a unique niche for immune reactions, extramedullary hematopoiesis, and the removal of aged erythrocytes from the circulation. While much is known about the immunological functions of the spleen, the mechanisms governing the development and organization of its stromal microenvironment remain poorly understood. Here we report the generation and analysis of a Tlx1 Cre ER ‐Venus knock‐in mouse strain engineered to simultaneously express tamoxifen‐inducible CreER T2 and Venus fluorescent protein under the control of regulatory elements of the Tlx1 gene, which encodes a transcription factor essential for spleen development. We demonstrated that Venus as well as CreER expression recapitulates endogenous Tlx1 transcription within the spleen microenvironment. When Tlx1 Cre ER ‐Venus mice were crossed with the Cre‐inducible reporter strain, Tlx1 ‐expressing cells as well as their descendants were specifically labeled following tamoxifen administration. We also showed by cell lineage tracing that asplenia caused by Tlx1 deficiency is attributable to altered contribution of mesenchymal cells in the spleen anlage to the pancreatic mesenchyme. Thus, Tlx1 Cre ER ‐Venus mice represent a new tool for lineage tracing and conditional gene manipulation of spleen mesenchymal cells, essential approaches for understanding the molecular mechanisms of spleen development. genesis 52:916–923, 2014. © 2014 Wiley Periodicals, Inc.