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Shlnc‐ EC 6 regulates murine erythroid enucleation by Rac1‐ PIP 5K pathway
Author(s) -
Wang Chenghai,
Wu Xiaohui,
Shen Feiyang,
Li Yaoyao,
Zhang Yanqing,
Yu Duonan
Publication year - 2015
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/dgd.12225
Subject(s) - gene knockdown , erythropoiesis , rac1 , haematopoiesis , rna , microbiology and biotechnology , biology , downregulation and upregulation , stem cell , chemistry , signal transduction , biochemistry , gene , medicine , anemia
Long noncoding RNA s (Lnc RNA s) are longer than 200 nucleotide noncoding RNA s without apparent functional coding capacity that function as regulators of cell growth and development. In recent years, increasing evidence implicates the involvement of Lnc RNA s in erythropoiesis. shlnc‐ EC 6 is a Lnc RNA associated with erythroid differentiation but the mechanism remains undefined. In this study, we found that knockdown of shlnc‐ EC 6 in purified mouse fetal liver erythroid progenitor and hematopoietic stem cells ( FLEPHSC s) significantly blocked erythroid enucleation. We also showed that Rac1 was negatively regulated by shlnc‐ EC 6 at the posttranscriptional level via specific binding to sites within the 3′ UTR of Rac1 m RNA . Moreover, we found that knockdown of shlnc‐ EC 6 led to upregulation of Rac1, followed by the activation of the downstream protein PIP 5K, and subsequently resulted in the inhibition of enucleation in cultured mouse fetal erythroblasts. Thus, our findings suggest that shlnc‐ EC 6 acts as a novel modulator to regulate mouse erythropoiesis via Rac1/ PIP 5K signaling pathway.