Yippee like 4 (Ypel4) is essential for normal mouse red blood cell membrane integrity

Autor: Abdul Ghani Alattar, Shamit Soneji, Ramprasad Ramakrishnan, Alexander Mattebo, Sofie Singbrant, Jenny Hansson, Johan Flygare, Stefan Lang, Emile van den Akker, Marcus Järås, Maria Jassinskaja, Kristýna Pimková, Isabel Prieto González-Albo, Taha Sen
Přispěvatelé: Landsteiner Laboratory
Rok vydání: 2021
Předmět:
Erythrocytes
Abnormal/metabolism
Male
Carrier Proteins/genetics
Erythrocytes
Abnormal/metabolism
Reticulocytosis
Inbred C57BL
Mice
Anion Exchange Protein 1
Erythrocyte
Erythropoiesis
Mice
Knockout
Multidisciplinary
Hematology
biology
Chemistry
Haematopoietic stem cells
Polycythemia/genetics
Anemia
Phenotype
Cell biology
Erythrocyte/metabolism
medicine.anatomical_structure
Erythrocytes/metabolism
Medicine
Female
medicine.symptom
medicine.medical_specialty
Knockout
Science
Erythrocytes
Abnormal
Spleen
Polycythemia
Anion Exchange Protein 1
Erythrocyte/metabolism
Article
Internal medicine
medicine
Animals
Anemia/metabolism
Gene
Band 3
Anion Exchange Protein 1
Erythrocyte Membrane
Erythropoiesis/genetics
Mice
Inbred C57BL
Erythrocyte Membrane/genetics
biology.protein
Bone marrow
Carrier Proteins
Zdroj: Scientific reports, 11(1). Nature Publishing Group
Scientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
Scientific Reports
ISSN: 2045-2322
DOI: 10.1038/s41598-021-95291-1
Popis: The YPEL family genes are highly conserved across a diverse range of eukaryotic organisms and thus potentially involved in essential cellular processes. Ypel4, one of five YPEL family gene orthologs in mouse and human, is highly and specifically expressed in late terminal erythroid differentiation (TED). In this study, we investigated the role of Ypel4 in murine erythropoiesis, providing for the first time an in-depth description of a Ypel4-null phenotype in vivo. We demonstrated that the Ypel4-null mice displayed a secondary polycythemia with macro- and reticulocytosis. While lack of Ypel4 did not affect steady-state TED in the bone marrow or spleen, the anemia-recovering capacity of Ypel4-null cells was diminished. Furthermore, Ypel4-null red blood cells (RBC) were cleared from the circulation at an increased rate, demonstrating an intrinsic defect of RBCs. Scanning electron micrographs revealed an ovalocytic morphology of Ypel4-null RBCs and functional testing confirmed reduced deformability. Even though Band 3 protein levels were shown to be reduced in Ypel4-null RBC membranes, we could not find support for a physical interaction between YPEL4 and the Band 3 protein. In conclusion, our findings provide crucial insights into the role of Ypel4 in preserving normal red cell membrane integrity.
Databáze: OpenAIRE
Externí odkaz: