Taz protects hematopoietic stem cells from an aging-dependent decrease in PU.1 activity

Kyung Mok Kim, Anna Mura-Meszaros, Marie Tollot, Murali Shyam Krishnan, Marco Gründl, Laura Neubert, Marco Groth, Alejo Rodriguez-Fraticelli, Arthur Flohr Svendsen, Stefano Campaner, Nico Andreas, Thomas Kamradt, Steve Hoffmann, Fernando D. Camargo, Florian H. Heidel, Leonid V. Bystrykh, Gerald Haan and Björn Eyss ()
Additional contact information
Kyung Mok Kim: Fritz Lipmann Institute e.V.
Anna Mura-Meszaros: Fritz Lipmann Institute e.V.
Marie Tollot: Fritz Lipmann Institute e.V.
Murali Shyam Krishnan: Fritz Lipmann Institute e.V.
Marco Gründl: Fritz Lipmann Institute e.V.
Laura Neubert: Fritz Lipmann Institute e.V.
Marco Groth: Fritz Lipmann Institute e.V.
Alejo Rodriguez-Fraticelli: Barcelona Institute of Science and Technology (BIST)
Arthur Flohr Svendsen: University of Groningen
Stefano Campaner: Fondazione Istituto Italiano di Tecnologia (IIT)
Nico Andreas: Jena University Hospital
Thomas Kamradt: Jena University Hospital
Steve Hoffmann: Fritz Lipmann Institute e.V.
Fernando D. Camargo: Barcelona Institute of Science and Technology (BIST)
Florian H. Heidel: Fritz Lipmann Institute e.V.
Leonid V. Bystrykh: University of Groningen
Gerald Haan: University of Groningen
Björn Eyss: Fritz Lipmann Institute e.V.

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract Specific functions of the immune system are essential to protect us from infections caused by pathogens such as viruses and bacteria. However, as we age, the immune system shows a functional decline that can be attributed in large part to age-associated defects in hematopoietic stem cells (HSCs)—the cells at the apex of the immune cell hierarchy. Here, we find that the Hippo pathway coactivator TAZ is potently induced in old HSCs and protects these cells from functional decline. We identify Clca3a1 as a TAZ-induced gene that allows us to trace TAZ activity in vivo. Using CLCA3A1 as a marker, we can isolate “young-like” HSCs from old mice. Mechanistically, Taz acts as coactivator of PU.1 and to some extent counteracts the gradual loss of PU.1 expression during HSC aging. Our work thus uncovers an essential role for Taz in a previously undescribed fail-safe mechanism in aging HSCs.

Date: 2022
References: View references in EconPapers View complete reference list from CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-022-32970-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-32970-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-022-32970-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().