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正常小脑发育及抑制髓母细胞瘤形成需要Dicer。

Dicer Is Required for Normal Cerebellar Development and to Restrain Medulloblastoma Formation.

作者信息

Zindy Frederique, Lee Youngsoo, Kawauchi Daisuke, Ayrault Olivier, Merzoug Leila Ben, Li Yang, McKinnon Peter J, Roussel Martine F

机构信息

Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN, United States of America.

Department of Genetics, St. Jude Children's Research Hospital, Memphis, TN, United States of America.

出版信息

PLoS One. 2015 Jun 19;10(6):e0129642. doi: 10.1371/journal.pone.0129642. eCollection 2015.

DOI:10.1371/journal.pone.0129642
PMID:26091048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4474721/
Abstract

Dicer, a ribonuclease III enzyme, is required for the maturation of microRNAs. To assess its role in cerebellar and medulloblastoma development, we genetically deleted Dicer in Nestin-positive neural progenitors and in mice lacking one copy for the Sonic Hedgehog receptor, Patched 1. We found that conditional loss of Dicer in mouse neural progenitors induced massive Trp53-independent apoptosis in all proliferative zones of the brain and decreased proliferation of cerebellar granule progenitors at embryonic day 15.5 leading to abnormal cerebellar development and perinatal lethality. Loss of one copy of Dicer significantly accelerated the formation of mouse medulloblastoma of the Sonic Hedgehog subgroup in Patched1-heterozygous mice. We conclude that Dicer is required for proper cerebellar development, and to restrain medulloblastoma formation.

摘要

Dicer是一种核糖核酸酶III，是微小RNA成熟所必需的。为了评估其在小脑和髓母细胞瘤发生发展中的作用，我们在巢蛋白阳性神经祖细胞以及缺乏一份音猬因子受体Patched 1的小鼠中通过基因手段删除了Dicer。我们发现，小鼠神经祖细胞中Dicer的条件性缺失在脑的所有增殖区诱导了大量不依赖Trp53的细胞凋亡，并在胚胎第15.5天降低了小脑颗粒祖细胞的增殖，导致小脑发育异常和围产期致死。在Patched1杂合小鼠中，一份Dicer的缺失显著加速了音猬因子亚组小鼠髓母细胞瘤的形成。我们得出结论，Dicer是小脑正常发育以及抑制髓母细胞瘤形成所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/3841aa8b98d4/pone.0129642.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/38bfa4f3abb2/pone.0129642.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/11b25ef204ee/pone.0129642.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/8224d4f0017f/pone.0129642.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/0807c909453a/pone.0129642.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/453df21376f6/pone.0129642.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/3841aa8b98d4/pone.0129642.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/38bfa4f3abb2/pone.0129642.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/11b25ef204ee/pone.0129642.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/8224d4f0017f/pone.0129642.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/0807c909453a/pone.0129642.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/453df21376f6/pone.0129642.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17e8/4474721/3841aa8b98d4/pone.0129642.g006.jpg

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