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对竹髓腔形成的形态解剖和细胞及转录组特征进行分析,揭示了与细胞程序性死亡相关基因的关键作用。

Morphological dissection and cellular and transcriptome characterizations of bamboo pith cavity formation reveal a pivotal role of genes related to programmed cell death.

机构信息

Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, Nanjing, Jiangsu, China.

Boyce Thompson Institute for Plant Research, Cornell University, Ithaca, NY, USA.

出版信息

Plant Biotechnol J. 2019 May;17(5):982-997. doi: 10.1111/pbi.13033. Epub 2018 Dec 9.

DOI:10.1111/pbi.13033
PMID:30451358
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6587456/
Abstract

Pith cavity formation is critical for bamboo to overcome the bending force during its fast growth; however, the underlying molecular mechanisms remain largely unknown. Multiple approaches, including anatomical dissection, mathematical modelling and transcriptome profiling, were employed in this study to investigate the biology of pith cavity formation in bamboo Pseudosasa japonica. We found that the corruption of pith tissue occurred sequentially and asymmetrically from the top-centre of the internode down to the bottom, which might be caused by the combined effects of asymmetrical radial and axial tensile forces during shoot-wall cell elongation and spiral growth of bamboo internodes. Programmed cell death (PCD) in pitch manifested by TUNEL positive nuclei, DNA cleavage and degraded organelles, and potentially regulated by ethylene and calcium signalling pathway, ROS burst, cell wall modification, proteolysis and nutrient recycle genes, might be responsible for pith tissue corruption of Ps. japonica. Although similar physiological changes and transcriptome profiles were found in different bamboo species, different formation rates of pith cavity were observed, which might be caused by different pith cells across the internode that were negatively correlated with the culm diameter. These findings provided a systematical view on the formation of bamboo pith cavity and revealed that PCD plays an important role in the bamboo pith cavity formation.

摘要

中空腔的形成对于竹子在快速生长过程中克服弯曲力至关重要;然而,其潜在的分子机制在很大程度上仍不清楚。本研究采用解剖学分析、数学建模和转录组分析等多种方法,研究了毛竹(Pseudosasa japonica)中空腔形成的生物学特性。我们发现,髓组织的腐败是从节间的顶部中心向底部依次、不对称地发生的,这可能是由于 shoot-wall 细胞伸长和竹子节间螺旋生长过程中产生的不对称径向和轴向拉伸力的共同作用所致。TUNEL 阳性核、DNA 断裂和降解的细胞器表明,管胞中的程序性细胞死亡(PCD)可能受乙烯和钙信号通路、ROS 爆发、细胞壁修饰、蛋白水解和养分循环基因的调控,这可能是导致 Ps. japonica 髓组织腐败的原因。尽管在不同的竹种中发现了类似的生理变化和转录组特征,但中空腔的形成速率不同,这可能是由于节间不同的髓细胞造成的,而髓细胞与竹秆直径呈负相关。这些发现为竹子中空腔的形成提供了一个系统的视角,并揭示了 PCD 在竹子中空腔形成过程中起着重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/3b72684c1ca4/PBI-17-982-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/afc69e989c43/PBI-17-982-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/9605ea558b1a/PBI-17-982-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/76ac5003c40e/PBI-17-982-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/4b3e9ee764dc/PBI-17-982-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/c2219ec6d235/PBI-17-982-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/7f843cbf8326/PBI-17-982-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/c5802f706c9a/PBI-17-982-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/7d9ef0e96f9a/PBI-17-982-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/3b72684c1ca4/PBI-17-982-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/afc69e989c43/PBI-17-982-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/9605ea558b1a/PBI-17-982-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/76ac5003c40e/PBI-17-982-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/4b3e9ee764dc/PBI-17-982-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/c2219ec6d235/PBI-17-982-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/7f843cbf8326/PBI-17-982-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/c5802f706c9a/PBI-17-982-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/7d9ef0e96f9a/PBI-17-982-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c4b/11386679/3b72684c1ca4/PBI-17-982-g006.jpg

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