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通过核层关联进行亚核基因定位会影响铜耐受性。

Subnuclear gene positioning through lamina association affects copper tolerance.

机构信息

Imaging Frontier Center, Organization for Research Advancement, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba, 278-8510, Japan.

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama-cho, Toyonaka, Osaka, 560-0043, Japan.

出版信息

Nat Commun. 2020 Nov 20;11(1):5914. doi: 10.1038/s41467-020-19621-z.

DOI:10.1038/s41467-020-19621-z
PMID:33219233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7679404/
Abstract

The nuclear lamina plays an important role in the regulation of chromatin organization and gene positioning in animals. CROWDED NUCLEI (CRWN) is a strong candidate for the plant nuclear lamina protein in Arabidopsis thaliana but its biological function was largely unknown. Here, we show that CRWNs localize at the nuclear lamina and build the meshwork structure. Fluorescence in situ hybridization and RNA-seq analyses revealed that CRWNs regulate chromatin distribution and gene expression. More than 2000 differentially expressed genes were identified in the crwn1crwn4 double mutant. Copper-associated (CA) genes that form a gene cluster on chromosome 5 were among the downregulated genes in the double mutant exhibiting low tolerance to excess copper. Our analyses showed this low tolerance to copper was associated with the suppression of CA gene expression and that CRWN1 interacts with the CA gene locus, enabling the locus to localize at the nuclear lamina under excess copper conditions.

摘要

核纤层在调节动物染色质组织和基因定位方面发挥着重要作用。在拟南芥中,CROWDED NUCLEI(CRWN)是核纤层蛋白的一个强有力的候选蛋白,但它的生物学功能在很大程度上是未知的。在这里,我们表明 CRWNs 定位于核纤层并构建网格结构。荧光原位杂交和 RNA-seq 分析表明,CRWNs 调节染色质分布和基因表达。在 crwn1crwn4 双突变体中鉴定出超过 2000 个差异表达基因。在双突变体中,铜相关(CA)基因是位于 5 号染色体上的基因簇的一部分,表现出对过量铜的低耐受性。我们的分析表明,这种对铜的低耐受性与 CA 基因表达的抑制有关,并且 CRWN1 与 CA 基因座相互作用,使该基因座能够在过量铜条件下定位在核纤层上。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/d9497343e0dd/41467_2020_19621_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/f1354801c684/41467_2020_19621_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/42d8043790cc/41467_2020_19621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/15aaa7a9dfcc/41467_2020_19621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/701d09dd83f5/41467_2020_19621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/d9497343e0dd/41467_2020_19621_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/f1354801c684/41467_2020_19621_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/42d8043790cc/41467_2020_19621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/15aaa7a9dfcc/41467_2020_19621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/701d09dd83f5/41467_2020_19621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/7679404/d9497343e0dd/41467_2020_19621_Fig5_HTML.jpg

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Loss of CRWN Nuclear Proteins Induces Cell Death and Salicylic Acid Defense Signaling.
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