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DEP1突变通过影响水稻细胞壁生物合成提高茎倒伏抗性和生物质糖化能力。

The DEP1 Mutation Improves Stem Lodging Resistance and Biomass Saccharification by Affecting Cell Wall Biosynthesis in Rice.

作者信息

Wang Ye, Wang Meihan, Yan Xia, Chen Kaixuan, Tian Fuhao, Yang Xiao, Cao Liyu, Ruan Nan, Dang Zhengjun, Yin Xuelin, Huang Yuwei, Li Fengcheng, Xu Quan

机构信息

Key Laboratory of Crop Physiology, Ecology, Genetics and Breeding, Ministry of Agriculture, Shenyang Agricultural University, Shenyang, China.

出版信息

Rice (N Y). 2024 May 15;17(1):35. doi: 10.1186/s12284-024-00712-0.

DOI:10.1186/s12284-024-00712-0
PMID:38748282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11096150/
Abstract

BACKGROUND

Plant cell walls have evolved precise plasticity in response to environmental stimuli. The plant heterotrimeric G protein complexes could sense and transmit extracellular signals to intracellular signaling systems, and activate a series of downstream responses. dep1 (Dense and Erect Panicles 1), the gain-of-function mutation of DEP1 encoding a G protein γ subunit, confers rice multiple improved agronomic traits. However, the effects of DEP1 on cell wall biosynthesis and wall-related agronomic traits remain largely unknown.

RESULTS

In this study, we showed that the DEP1 mutation affects cell wall biosynthesis, leading to improved lodging resistance and biomass saccharification. The DEP1 is ubiquitously expressed with a relatively higher expression level in tissues rich in cell walls. The CRISPR/Cas9 editing mutants of DEP1 (dep1-cs) displayed a significant enhancement in stem mechanical properties relative to the wild-type, leading to a substantial improvement in lodging resistance. Cell wall analyses showed that the DEP1 mutation increased the contents of cellulose, hemicelluloses, and pectin, and reduced lignin content and cellulose crystallinity (CrI). Additionally, the dep1-cs seedlings exhibited higher sensitivity to cellulose biosynthesis inhibitors, 2,6-Dichlorobenzonitrile (DCB) and isoxaben, compared with the wild-type, confirming the role of DEP1 in cellulose deposition. Moreover, the DEP1 mutation-mediated alterations of cell walls lead to increased enzymatic saccharification of biomass after the alkali pretreatment. Furthermore, the comparative transcriptome analysis revealed that the DEP1 mutation substantially altered expression of genes involved in carbohydrate metabolism, and cell wall biosynthesis.

CONCLUSIONS

Our findings revealed the roles of DEP1 in cell wall biosynthesis, lodging resistance, and biomass saccharification in rice and suggested genetic modification of DEP1 as a potential strategy to develop energy rice varieties with high lodging resistance.

摘要

背景

植物细胞壁在响应环境刺激时进化出了精确的可塑性。植物异源三聚体G蛋白复合物能够感知细胞外信号并将其传递到细胞内信号系统,进而激活一系列下游反应。dep1(密穗直立穗1)是编码G蛋白γ亚基的DEP1功能获得性突变体,赋予水稻多种优良农艺性状。然而,DEP1对细胞壁生物合成及与细胞壁相关的农艺性状的影响仍知之甚少。

结果

在本研究中,我们发现DEP1突变影响细胞壁生物合成,从而提高了抗倒伏性和生物质糖化能力。DEP1在各处均有表达,在富含细胞壁的组织中表达水平相对较高。DEP1的CRISPR/Cas9编辑突变体(dep1-cs)相对于野生型,茎的机械性能显著增强,抗倒伏性大幅提高。细胞壁分析表明,DEP1突变增加了纤维素、半纤维素和果胶的含量,降低了木质素含量和纤维素结晶度(CrI)。此外,与野生型相比,dep1-cs幼苗对纤维素生物合成抑制剂2,6-二氯苯腈(DCB)和异恶草酮表现出更高的敏感性,证实了DEP1在纤维素沉积中的作用。而且,DEP1突变介导的细胞壁改变导致碱预处理后生物质的酶促糖化增加。此外,比较转录组分析显示,DEP1突变显著改变了参与碳水化合物代谢和细胞壁生物合成的基因表达。

结论

我们的研究结果揭示了DEP1在水稻细胞壁生物合成、抗倒伏性和生物质糖化中的作用,并表明对DEP1进行基因改造是培育高抗倒伏性能源水稻品种的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/8aba6f118f2f/12284_2024_712_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/d6bd48a57ba0/12284_2024_712_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/19c608e2f570/12284_2024_712_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/d813308e5f3b/12284_2024_712_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/5b7690b51389/12284_2024_712_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/bcebf0cc8e6e/12284_2024_712_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/c59d3e286bf3/12284_2024_712_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/eee19d42a45a/12284_2024_712_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/8aba6f118f2f/12284_2024_712_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/d6bd48a57ba0/12284_2024_712_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/3f26458fcf57/12284_2024_712_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/19c608e2f570/12284_2024_712_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/d813308e5f3b/12284_2024_712_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/5b7690b51389/12284_2024_712_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/bcebf0cc8e6e/12284_2024_712_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/c59d3e286bf3/12284_2024_712_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/eee19d42a45a/12284_2024_712_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733a/11096150/8aba6f118f2f/12284_2024_712_Fig9_HTML.jpg

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