scholarly journals An integrative analysis of the transcriptome and proteome of the pulp of a spontaneous late-ripening sweet orange mutant and its wild type improves our understanding of fruit ripening in citrus

2014 ◽  
Vol 65 (6) ◽  
pp. 1651-1671 ◽  
Author(s):  
Juxun Wu ◽  
Zhilong Xu ◽  
Yajian Zhang ◽  
Lijun Chai ◽  
Hualin Yi ◽  
...  
2022 ◽  
Vol 294 ◽  
pp. 110786
Author(s):  
Lifang Sun ◽  
Nasrullah ◽  
Fuzhi Ke ◽  
Zhenpeng Nie ◽  
Jianguo Xu ◽  
...  

2020 ◽  
Vol 71 (12) ◽  
pp. 3560-3574 ◽  
Author(s):  
Ying Gao ◽  
Wei Wei ◽  
Zhongqi Fan ◽  
Xiaodan Zhao ◽  
Yiping Zhang ◽  
...  

Abstract The tomato non-ripening (nor) mutant generates a truncated 186-amino-acid protein (NOR186) and has been demonstrated previously to be a gain-of-function mutant. Here, we provide more evidence to support this view and answer the open question of whether the NAC-NOR gene is important in fruit ripening. Overexpression of NAC-NOR in the nor mutant did not restore the full ripening phenotype. Further analysis showed that the truncated NOR186 protein is located in the nucleus and binds to but does not activate the promoters of 1-aminocyclopropane-1-carboxylic acid synthase2 (SlACS2), geranylgeranyl diphosphate synthase2 (SlGgpps2), and pectate lyase (SlPL), which are involved in ethylene biosynthesis, carotenoid accumulation, and fruit softening, respectively. The activation of the promoters by the wild-type NOR protein can be inhibited by the mutant NOR186 protein. On the other hand, ethylene synthesis, carotenoid accumulation, and fruit softening were significantly inhibited in CR-NOR (CRISPR/Cas9-edited NAC-NOR) fruit compared with the wild-type, but much less severely affected than in the nor mutant, while they were accelerated in OE-NOR (overexpressed NAC-NOR) fruit. These data further indicated that nor is a gain-of-function mutation and NAC-NOR plays a significant role in ripening of wild-type fruit.


2013 ◽  
Vol 150 (2) ◽  
pp. 252-270 ◽  
Author(s):  
Yunliu Zeng ◽  
Zhiyong Pan ◽  
Lun Wang ◽  
Yuduan Ding ◽  
Qiang Xu ◽  
...  
Keyword(s):  

BMC Genomics ◽  
2010 ◽  
Vol 11 (1) ◽  
pp. 246 ◽  
Author(s):  
Qiang Xu ◽  
Yuanlong Liu ◽  
Andan Zhu ◽  
Xiaomeng Wu ◽  
Junli Ye ◽  
...  
Keyword(s):  

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Mengting Pi ◽  
Shaoqiang Hu ◽  
Laichao Cheng ◽  
Ruhan Zhong ◽  
Zhuoying Cai ◽  
...  

AbstractFlower and fruit development are two key steps for plant reproduction. The ABCE model for flower development has been well established in model plant species; however, the functions of ABCE genes in fruit crops are less understood. In this work, we identified an EMS mutant named R27 in woodland strawberry (Fragaria vesca), showing the conversion of petals, stamens, and carpels to sepaloid organs in a semidominant inheritance fashion. Mapping by sequencing revealed that the class E gene homolog FveSEP3 (FvH4_4g23530) possessed the causative mutation in R27 due to a G to E amino acid change in the conserved MADS domain. Additional fvesep3CR mutants generated by CRISPR/Cas9 displayed similar phenotypes to fvesep3-R27. Overexpressing wild-type or mutated FveSEP3 in Arabidopsis suggested that the mutation in R27 might cause a dominant-negative effect. Further analyses indicated that FveSEP3 physically interacted with each of the ABCE proteins in strawberry. Moreover, both R27 and fvesep3CR mutants exhibited parthenocarpic fruit growth and delayed fruit ripening. Transcriptome analysis revealed that both common and specific differentially expressed genes were identified in young fruit at 6–7 days post anthesis (DPA) of fvesep3 and pollinated wild type when compared to unpollinated wild type, especially those in the auxin pathway, a key hormone regulating fruit set in strawberry. Together, we provided compelling evidence that FveSEP3 plays predominant E functions compared to other E gene homologs in flower development and that FveSEP3 represses fruit growth in the absence of pollination and promotes fruit ripening in strawberry.


Author(s):  
Jie Song ◽  
Hao Wu ◽  
Feng He ◽  
Jing Qu ◽  
Yue Wang ◽  
...  

Abstract C-repeat (CRT) binding factors (CBFs) are well known to act as crucial transcription factors that function in cold stress response. Arginine decarboxylase (ADC)-mediated putrescine biosynthesis has been reported to be activated in plants exposed to cold conditions, but it remains elusive whether CBFs can regulate ADC expression and putrescine accumulation. In this study, we show that cold up-regulated ADC gene (CsADC) and elevation of endogenous putrescine content in sweet orange (Citrus sinensis). Promoter of CsADC contains two CRT sequences that are canonical elements recognized by CBFs. Sweet orange genome contains four CBFs (CsCBF1-4), in which CsCBF1 was significantly induced by cold. CsCBF1, located in the nucleus, was demonstrated to bind directly and specifically to the promoter of CsADC and acted as a transcriptional activator. Overexpression of CsCBF1 led to notable elevation of CsADC and putrescine level in sweet orange transgenic plants, along with remarkably enhanced cold tolerance, relative to the wild type (WT). However, pretreatment with D-arginine, an ADC inhibitor, caused prominent reduction of endogenous putrescine level in the overexpressing lines, accompanied by greatly compromised cold tolerance. Taken together, these results demonstrate that CBF1 of sweet orange directly regulates ADC expression and modulates putrescine synthesis for orchestrating the cold tolerance. Our findings shed light into the transcriptional regulation of putrescine accumulation through targeting the ADC gene in the presence of cold stress. Meanwhile, this study illustrates a new mechanism underlying the CBF-mediated cold stress response.


Sign in / Sign up

Export Citation Format

Share Document