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萘乙酸诱导茶树插条不定根形成的转录组和激素分析。

Integrated transcriptome and hormonal analysis of naphthalene acetic acid-induced adventitious root formation of tea cuttings (Camellia sinensis).

机构信息

Key Laboratory of Tea Biology and Resources Utilization, Ministry of Agriculture, National Center for Tea Improvement, Tea Research Institute Chinese Academy of Agricultural Sciences (TRICAAS), Hangzhou, 310008, China.

Tea Research Institute, Yunnan Academy of Agricultural Sciences, Menghai, 666201, China.

出版信息

BMC Plant Biol. 2022 Jul 4;22(1):319. doi: 10.1186/s12870-022-03701-x.

DOI:10.1186/s12870-022-03701-x
PMID:35787241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9251942/
Abstract

BACKGROUND

Tea plant breeding or cultivation mainly involves propagation via cuttings, which not only ensures the inheritance of the excellent characteristics of the mother plant but also facilitates mechanized management. The formation of adventitious root (AR) determines the success of cutting-based propagation, and auxin is an essential factor involved in this process. To understand the molecular mechanism underlying AR formation in nodal tea cuttings, transcriptome and endogenous hormone analysis was performed on the stem bases of red (mature)- and green (immature)-stem cuttings of 'Echa 1 hao' tea plant as affected by a pulse treatment with naphthalene acetic acid (NAA).

RESULTS

In this study, NAA significantly promoted AR formation in both red- and green-stem cuttings but slightly reduced callus formation. External application of NAA reduced the levels of endogenous indole-3-acetic acid (IAA) and cytokinin (TZR, trans-zeatin riboside). The number of DEGs (NAA vs. CK) identified in the green-stem cuttings was significantly higher than that in the red-stem cuttings, which corresponded to a higher rooting rate of green-stem cuttings under the NAA treatment. A total of 82 common DEGs were identified as being hormone-related and involved in the auxin, cytokinin, abscisic acid, ethylene, salicylic acid, brassinosteroid, and jasmonic acid pathways. The negative regulation of NAA-induced IAA and GH3 genes may explain the decrease of endogenous IAA. NAA reduced endogenous cytokinin levels and further downregulated the expression of cytokinin signalling-related genes. By the use of weighted gene co-expression network analysis (WGCNA), several hub genes, including three [cellulose synthase (CSLD2), SHAVEN3-like 1 (SVL1), SMALL AUXIN UP RNA (SAUR21)] that are highly related to root development in other crops, were identified that might play important roles in AR formation in tea cuttings.

CONCLUSIONS

NAA promotes the formation of AR of tea cuttings in coordination with endogenous hormones. The most important endogenous AR inductor, IAA, was reduced in response to NAA. DEGs potentially involved in NAA-mediated AR formation of tea plant stem cuttings were identified via comparative transcriptome analysis. Several hub genes, such as CSLD2, SVL1 and SAUR21, were identified that might play important roles in AR formation in tea cuttings.

摘要

背景

茶树的育种或栽培主要涉及通过插条进行繁殖,这不仅确保了母株优良特性的遗传,而且便于机械化管理。不定根(AR)的形成决定了基于切割的繁殖的成功,而生长素是参与该过程的一个必要因素。为了了解节点茶树插条中 AR 形成的分子机制,对‘Echa 1 hao’茶树的红(成熟)茎和绿(不成熟)茎插条的茎基部进行了转录组和内源激素分析,这些插条受到萘乙酸(NAA)脉冲处理的影响。

结果

在这项研究中,NAA 显著促进了红茎和绿茎插条中 AR 的形成,但轻微减少了愈伤组织的形成。NAA 的外部应用降低了内源吲哚-3-乙酸(IAA)和细胞分裂素(TZR,反式玉米素核苷)的水平。在绿茎插条中鉴定的差异表达基因(NAA 与 CK)的数量明显高于红茎插条,这对应于 NAA 处理下绿茎插条更高的生根率。总共鉴定出 82 个共同的差异表达基因与激素有关,参与生长素、细胞分裂素、脱落酸、乙烯、水杨酸、油菜素内酯和茉莉酸途径。NAA 诱导的 IAA 和 GH3 基因的负调控可能解释了内源 IAA 的减少。NAA 降低了内源细胞分裂素水平,并进一步下调了细胞分裂素信号相关基因的表达。通过使用加权基因共表达网络分析(WGCNA),鉴定了几个枢纽基因,包括三个与其他作物根发育高度相关的基因[纤维素合酶(CSLD2)、SHAVEN3 样 1(SVL1)、小生长素 UP RNA(SAUR21)],它们可能在茶树插条的 AR 形成中发挥重要作用。

结论

NAA 与内源激素协同促进茶树插条 AR 的形成。最重要的内源 AR 诱导剂 IAA 对 NAA 有反应。通过比较转录组分析,鉴定了可能参与茶树茎切段 NAA 介导的 AR 形成的差异表达基因。鉴定了几个枢纽基因,如 CSLD2、SVL1 和 SAUR21,它们可能在茶树插条的 AR 形成中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/fd6b45b0c4e1/12870_2022_3701_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/fd6b45b0c4e1/12870_2022_3701_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/636e3a191474/12870_2022_3701_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/ae7e2a906e47/12870_2022_3701_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/acc2ff2127b0/12870_2022_3701_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/71a4a9b5398b/12870_2022_3701_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/38e94b7ab008/12870_2022_3701_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/d7c816e8cb12/12870_2022_3701_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/9c8def9303c0/12870_2022_3701_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/114511edffdc/12870_2022_3701_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0166/9251942/fd6b45b0c4e1/12870_2022_3701_Fig9_HTML.jpg

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