TY - JOUR
T1 - Gene expression profiling in neuronal cells identifies a different type of transcriptome modulated by NF-Y
AU - Yamanaka, Tomoyuki
AU - Miyazaki, Haruko
AU - Tosaki, Asako
AU - Maity, Sankar N.
AU - Shimogori, Tomomi
AU - Hattori, Nobutaka
AU - Nukina, Nobuyuki
N1 - Funding Information:
We thank Mrs Itsuko Yamamoto for mice maintenance and sampling, Support Unit for Bio-Material Analysis of RIKEN CBS, especially Dr Kenji Ohtawa and Dr Keisuke Fukumoto for FACS sorting, RNA-seq and DNA microarray analyses. We also thank lab members of RIKEN CBS, Juntendo University and Doshisha University for helpful discussions. This work was supported by a Grant-in-Aid from Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan for T.Y. (18H02723, 17KT0131, 15K06762) and N.N. (17H01564, 16H01345, 15H01567), Takeda Science Foundation, The Sumitomo Foundation, and Center for Baby Science in Doshisha University (Joint Usage/Research Center for accredited by MEXT). This work is partially supported by the Strategic Research Program for Brain Sciences from Japan Agency for Medical Research and Development, AMED.
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/12
Y1 - 2020/12
N2 - A heterotrimeric transcription factor NF-Y is crucial for cell-cycle progression in various types of cells. In contrast, studies using NF-YA knockout mice have unveiled its essential role in endoplasmic reticulum (ER) homeostasis in neuronal cells. However, whether NF-Y modulates a different transcriptome to mediate distinct cellular functions remains obscure. Here, we knocked down NF-Y in two types of neuronal cells, neuro2a neuroblastoma cells and mouse brain striatal cells, and performed gene expression profiling. We found that down-regulated genes preferentially contained NF-Y-binding motifs in their proximal promoters, and notably enriched genes related to ER functions rather than those for cell cycle. This contrasts with the profiling data of HeLa and embryonic stem cells in which distinct down-regulation of cell cycle-related genes was observed. Clustering analysis further identified several functional clusters where populations of the down-regulated genes were highly distinct. Further analyses using chromatin immunoprecipitation and RNA-seq data revealed that the transcriptomic difference was not correlated with DNA binding of NF-Y but with splicing of NF-YA. These data suggest that neuronal cells have a different type of transcriptome in which ER-related genes are dominantly modulated by NF-Y, and imply that NF-YA splicing alteration could be involved in this cell type-specific gene modulation.
AB - A heterotrimeric transcription factor NF-Y is crucial for cell-cycle progression in various types of cells. In contrast, studies using NF-YA knockout mice have unveiled its essential role in endoplasmic reticulum (ER) homeostasis in neuronal cells. However, whether NF-Y modulates a different transcriptome to mediate distinct cellular functions remains obscure. Here, we knocked down NF-Y in two types of neuronal cells, neuro2a neuroblastoma cells and mouse brain striatal cells, and performed gene expression profiling. We found that down-regulated genes preferentially contained NF-Y-binding motifs in their proximal promoters, and notably enriched genes related to ER functions rather than those for cell cycle. This contrasts with the profiling data of HeLa and embryonic stem cells in which distinct down-regulation of cell cycle-related genes was observed. Clustering analysis further identified several functional clusters where populations of the down-regulated genes were highly distinct. Further analyses using chromatin immunoprecipitation and RNA-seq data revealed that the transcriptomic difference was not correlated with DNA binding of NF-Y but with splicing of NF-YA. These data suggest that neuronal cells have a different type of transcriptome in which ER-related genes are dominantly modulated by NF-Y, and imply that NF-YA splicing alteration could be involved in this cell type-specific gene modulation.
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U2 - 10.1038/s41598-020-78682-8
DO - 10.1038/s41598-020-78682-8
M3 - Article
C2 - 33303918
AN - SCOPUS:85097363768
SN - 2045-2322
VL - 10
JO - Scientific Reports
JF - Scientific Reports
IS - 1
M1 - 21714
ER -