Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014 Nov;52(11):916-23.
doi: 10.1002/dvg.22829. Epub 2014 Oct 18.

Generation of a Tlx1(CreER-Venus) knock-in mouse strain for the study of spleen development

Ryo Nakahara  1 , Yasuhiro Kawai, Akihisa Oda, Miyuki Nishimura, Akikazu Murakami, Takachika Azuma, Tomonori Kaifu, Ryo Goitsuka
Affiliations

Generation of a Tlx1(CreER-Venus) knock-in mouse strain for the study of spleen development

Ryo Nakahara et al. Genesis. 2014 Nov.

Abstract

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.

Keywords: Tlx1; Venus; lineage tracing; mouse; spleen; tamoxifen-inducible Cre.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

Publication types

MeSH terms

LinkOut - more resources