کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8309083 | 1538502 | 2018 | 56 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Overexpression of dJmj differentially affects intestinal stem cells and differentiated enterocytes
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کلمات کلیدی
PRC2YorkieISCsH3K27me3EESEBsJnkEGFRc-Jun N-terminal kinase - C-Jun N-terminal kinaseECs - EC هاJAK/STAT - JAK / STATEnterocytes - انتروسی هاSuppressor of Hairless - سرکوب کننده بی موintestinal stem cells - سلول های بنیادی رودهenteroendocrine cells - سلولهای enteroendocrineSu(H) - سو (H)polycomb repressive complex 2 - پیچک سرکوبگر پلی کامب 2janus kinase/signal transducer and activator of transcription - ژنوس کیناز / فرستنده سیگنال و فعال کننده رونویسیEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمالYki - یکی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Jumonji (Jmj)/Jarid2 is a DNA-binding transcriptional repressor mediated via histone methylation. Nevertheless, the well-known function of Jmj is as a scaffold for the recruitment of various complexes including Polycomb repressive complex 2 (PRC2), and required for mouse embryonic stem cell development. However, PRC2 independent function is suggested for Drosophila Jumonji (dJmj). To clarify the function of dJmj during cell differentiation, we used Drosophila adult intestinal stem cell system that allows to follow stem cell behaviors in vivo. Overexpression of dJmj in intestinal stem cells/enteroblasts (ISCs/EBs) induces cell-autonomous ISC proliferation followed by differentiation, that is controlled by the Notch and EGFR pathway. In contrast, overexpression of dJmj in enterocytes (ECs) resulted in activation of the JNK pathway in ECs followed by the induction of apoptosis. Activated JNK increased the level of Yorkie in ECs and induced the reduction of Upd proteins and EGFR ligands, which activated the JAK/STAT and EGFR pathway in both ISCs and EBs to promote ISC proliferation. The Notch signaling pathway appears to be highly activated to support the differentiation of EBs to ECs. Thus, the combination of these signaling pathways caused by ECs-specific dJmj-overexpression induced non-cell-autonomous ISC proliferation and differentiation. Surprisingly, these effects did not relate to H3K27me3 status, likely represented PRC2 activity, in cells that overexpressed dJmj. Instead of this, the disappearance of H3K27me3 in ISC/EB-specific overexpressed dJmj suggested a possible PRC2-independent role of dJmj in regulating chromatin structure.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 42, January 2018, Pages 194-210
Journal: Cellular Signalling - Volume 42, January 2018, Pages 194-210
نویسندگان
Dang Ngoc Anh Suong, Kouhei Shimaji, Jung-Hoon Pyo, Joung-Sun Park, Hideki Yoshida, Mi-Ae Yoo, Masamitsu Yamaguchi,