scholarly journals The apple MdCOP1-interacting protein 1 negatively regulates hypocotyl elongation and anthocyanin biosynthesis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hui Kang ◽  
Ting-Ting Zhang ◽  
Lu-Lu Fu ◽  
Yu-Xin Yao ◽  
Chun-Xiang You ◽  
...  

Abstract Background In plants, CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) is a key negative regulator in photoperiod response. However, the biological function of COP1-interacting protein 1 (CIP1) and the regulatory mechanism of the CIP1-COP1 interaction are not fully understood. Results Here, we identified the apple MdCIP1 gene based on the Arabidopsis AtCIP1 gene. Expression pattern analysis showed that MdCIP1 was constitutively expressed in various tissues of apple, and responded to stress and hormone signals at the transcriptional level. Ectopic expression of MdCIP1 complemented the phenotypes of the Arabidopsis cip1 mutant, and MdCIP1 inhibited anthocyanin biosynthesis in apple calli. In addition, the biochemical assay demonstrated that MdCIP1 could interact with MdCOP1 protein by their coiled-coil domain, and MdCIP1-OX/cop1–4 had a similar phenotype in photomorphogenesis with the cop1–4 mutant, suggesting that COP1 is epistatic to CIP1. Furthermore, the transient transformation assay indicated that MdCIP1 repressed anthocyanin biosynthesis in an MdCOP1-mediated pathway. Conclusion Take together, this study finds that MdCIP1 acts as a repressor in regulating hypocotyl elongation and anthocyanin biosynthesis through MdCOP1 in apple.

2019 ◽  
Vol 61 (1) ◽  
pp. 130-143 ◽  
Author(s):  
Jian-Ping An ◽  
Xiao-Fei Wang ◽  
Richard V Espley ◽  
Kui Lin-Wang ◽  
Si-Qi Bi ◽  
...  

Abstract As an important environment factor, light affects plant growth and development throughout life. B-BOX (BBX) proteins play key roles in the regulation of light signaling. Although the multiple roles of BBX proteins have been extensively studied in Arabidopsis, the research in apple is much less extensive. In this study, we systematically characterized the negative role of an apple BBX protein MdBBX37 in light signaling, including inhibiting anthocyanin biosynthesis and promoting hypocotyl elongation. We found that MdBBX37 interacted with MdMYB1 and MdMYB9, two key positive regulators of anthocyanin biosynthesis, and inhibited the binding of those two proteins to their target genes and, therefore, negatively regulated anthocyanin biosynthesis. In addition, MdBBX37 directly bound to the promoter of MdHY5, a positive regulator of light signaling, and suppressed its expression, and thus relieved MdHY5-mediated hypocotyl inhibition. Taken together, our investigations suggest that MdBBX37 is a negative regulator of light signaling in apple. Our study will provide reference for further study on the functions of BBX proteins in apple.


2021 ◽  
Author(s):  
Dongming Zhao ◽  
Yuxuan Zheng ◽  
lingjun Yang ◽  
Ziyu Yao ◽  
Jianfeng Cheng ◽  
...  

Abstract Background: The regulation of anthocyanin biosynthesis by various factors including sugars, light and abiotic stresses is mediated by numerous regulatory factors acting at the transcriptional level. Here experimental evidence was provided in order to demonstrate that the nuclear GARP transcription factor AtGLK1 plays an important role in regulating sucrose-induced anthocyanin biosynthesis in Arabidopsis.Results: The results obtained using real-time quantitative PCR and GUS staining assays revealed that AtGLK1 was mainly expressed in the green tissues of Arabidopsis seedlings and could be induced by sucrose. The loss-of-function glk1 glk2 double mutant has lower anthocyanin levels than the glk2 single mutant, although it has been determined that loss of AtGLK1 alone does not affect anthocyanin accumulation. Overexpression of AtGLK1 enhances the accumulation of anthocyanin in transgenic Arabidopsis seedlings accompanied by increased expression of anthocyanin biosynthetic and regulatory genes. Moreover, we found that AtGLK1 also participates in plastid-signaling mediated anthocyanin accumulations. Genetic, physiological, and molecular biological approaches demonstrated that AtGLK1 acts upstream of MYBL2, which is a key negative regulator of anthocyanin biosynthesis, to genetically regulate sucrose-induced anthocyanin biosynthesis.Conclusion: Our results indicated that AtGLK1 positively regulates sucrose-induced anthocyanin biosynthesis in Arabidopsis via MYBL2.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dongming Zhao ◽  
Yuxuan Zheng ◽  
lingjun Yang ◽  
Ziyu Yao ◽  
Jianfeng Cheng ◽  
...  

Abstract Background The regulation of anthocyanin biosynthesis by various factors including sugars, light and abiotic stresses is mediated by numerous regulatory factors acting at the transcriptional level. Here experimental evidence was provided in order to demonstrate that the nuclear GARP transcription factor AtGLK1 plays an important role in regulating sucrose-induced anthocyanin biosynthesis in Arabidopsis. Results The results obtained using real-time quantitative PCR and GUS staining assays revealed that AtGLK1 was mainly expressed in the green tissues of Arabidopsis seedlings and could be induced by sucrose. The loss-of-function glk1 glk2 double mutant has lower anthocyanin levels than the glk2 single mutant, although it has been determined that loss of AtGLK1 alone does not affect anthocyanin accumulation. Overexpression of AtGLK1 enhances the accumulation of anthocyanin in transgenic Arabidopsis seedlings accompanied by increased expression of anthocyanin biosynthetic and regulatory genes. Moreover, we found that AtGLK1 also participates in plastid-signaling mediated anthocyanin accumulations. Genetic, physiological, and molecular biological approaches demonstrated that AtGLK1 acts upstream of MYBL2, which is a key negative regulator of anthocyanin biosynthesis, to genetically regulate sucrose-induced anthocyanin biosynthesis. Conclusion Our results indicated that AtGLK1 positively regulates sucrose-induced anthocyanin biosynthesis in Arabidopsis via MYBL2.


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Weihao Wang ◽  
Peiwen Wang ◽  
Xiaojing Li ◽  
Yuying Wang ◽  
Shiping Tian ◽  
...  

AbstractLight plays a critical role in plant growth and development, but the mechanisms through which light regulates fruit ripening and nutritional quality in horticultural crops remain largely unknown. Here, we found that ELONGATED HYPOCOTYL 5 (HY5), a master regulator in the light signaling pathway, is required for normal fruit ripening in tomato (Solanum lycopersicum). Loss of function of tomato HY5 (SlHY5) impairs pigment accumulation and ethylene biosynthesis. Transcriptome profiling identified 2948 differentially expressed genes, which included 1424 downregulated and 1524 upregulated genes, in the Slhy5 mutants. In addition, genes involved in carotenoid and anthocyanin biosynthesis and ethylene signaling were revealed as direct targets of SlHY5 by chromatin immunoprecipitation. Surprisingly, the expression of a large proportion of genes encoding ribosomal proteins was downregulated in the Slhy5 mutants, and this downregulation pattern was accompanied by a decrease in the abundance of ribosomal proteins. Further analysis demonstrated that SlHY5 affected the translation efficiency of numerous ripening-related genes. These data indicate that SlHY5 regulates fruit ripening both at the transcriptional level by targeting specific molecular pathways and at the translational level by affecting the protein translation machinery. Our findings unravel the regulatory mechanisms of SlHY5 in controlling fruit ripening and nutritional quality and uncover the multifaceted regulation of gene expression by transcription factors.


Plants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 323
Author(s):  
Sujuan Shi ◽  
Lulu An ◽  
Jingjing Mao ◽  
Oluwaseun Olayemi Aluko ◽  
Zia Ullah ◽  
...  

CBL-interacting protein kinase (CIPK) family is a unique group of serine/threonine protein kinase family identified in plants. Among this family, AtCIPK23 and its homologs in some plants are taken as a notable group for their importance in ions transport and stress responses. However, there are limited reports on their roles in seedling growth and development, especially in Solanaceae plants. In this study, NtCIPK23, a homolog of AtCIPK23 was cloned from Nicotiana tabacum. Expression analysis showed that NtCIPK23 is mainly expressed in the radicle, hypocotyl, and cotyledons of young tobacco seedlings. The transcriptional level of NtCIPK23 changes rapidly and spatiotemporally during seed germination and early seedling growth. To study the biological function of NtCIPK23 at these stages, the overexpressing and CRISPR/Cas9-mediated knock-out (ntcipk23) tobacco lines were generated. Phenotype analysis indicated that knock-out of NtCIPK23 significantly delays seed germination and the appearance of green cotyledon of young tobacco seedling. Overexpression of NtCIPK23 promotes cotyledon expansion and hypocotyl elongation of young tobacco seedlings. The expression of NtCIPK23 in hypocotyl is strongly upregulated by darkness and inhibited under light, suggesting that a regulatory mechanism of light might underlie. Consistently, a more obvious difference in hypocotyl length among different tobacco materials was observed in the dark, compared to that under the light, indicating that the upregulation of NtCIPK23 contributes greatly to the hypocotyl elongation. Taken together, NtCIPK23 not only enhances tobacco seed germination, but also accelerate early seedling growth by promoting cotyledon greening rate, cotyledon expansion and hypocotyl elongation of young tobacco seedlings.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Min Ji Yoon ◽  
Boyoon Choi ◽  
Eun Jin Kim ◽  
Jiyeon Ohk ◽  
Chansik Yang ◽  
...  

Abstractp62/SQSTM1 is known to act as a key mediator in the selective autophagy of protein aggregates, or aggrephagy, by steering ubiquitinated protein aggregates towards the autophagy pathway. Here, we use a yeast two-hybrid screen to identify the prefoldin-like chaperone UXT as an interacting protein of p62. We show that UXT can bind to protein aggregates as well as the LB domain of p62, and, possibly by forming an oligomer, increase p62 clustering for its efficient targeting to protein aggregates, thereby promoting the formation of the p62 body and clearance of its cargo via autophagy. We also find that ectopic expression of human UXT delays SOD1(A4V)-induced degeneration of motor neurons in a Xenopus model system, and that specific disruption of the interaction between UXT and p62 suppresses UXT-mediated protection. Together, these results indicate that UXT functions as an autophagy adaptor of p62-dependent aggrephagy. Furthermore, our study illustrates a cooperative relationship between molecular chaperones and the aggrephagy machinery that efficiently removes misfolded protein aggregates.


2021 ◽  
Vol 12 (1) ◽  
pp. 009-019
Author(s):  
Ying Yang ◽  
Jin Wang ◽  
Shihai Xu ◽  
Wen Lv ◽  
Fei Shi ◽  
...  

Abstract Background In cancer, kappa B-interacting protein (IKBIP) has rarely been reported. This study aimed at investigating its expression pattern and biological function in brain glioma at the transcriptional level. Methods We selected 301 glioma patients with microarray data from CGGA database and 697 glioma patients with RNAseq data from TCGA database. Transcriptional data and clinical data of 998 samples were analyzed. Statistical analysis and figure generating were performed with R language. Results We found that IKBIP expression showed positive correlation with WHO grade of glioma. IKBIP was increased in isocitrate dehydrogenase (IDH) wild type and mesenchymal molecular subtype of glioma. Gene ontology analysis demonstrated that IKBIP was profoundly associated with extracellular matrix organization, cell–substrate adhesion and response to wounding in both pan-glioma and glioblastoma. Subsequent gene set enrichment analysis revealed that IKBIP was particularly correlated with epithelial-to-mesenchymal transition (EMT). To further elucidate the relationship between IKBIP and EMT, we performed gene set variation analysis to screen the EMT-related signaling pathways and found that IKBIP expression was significantly associated with PI3K/AKT, hypoxia and TGF-β pathway. Moreover, IKBIP expression was found to be synergistic with key biomarkers of EMT, especially with N-cadherin, vimentin, snail, slug and TWIST1. Finally, higher IKBIP indicated significantly shorter survival for glioma patients. Conclusions IKBIP was associated with more aggressive phenotypes of gliomas. Furthermore, IKBIP was significantly involved in EMT and could serve as an independent prognosticator in glioma.


Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 131-141
Author(s):  
Laurent Molin ◽  
Heinke Schnabel ◽  
Titus Kaletta ◽  
Richard Feichtinger ◽  
Ian A Hope ◽  
...  

Abstract In the early Caenorhabditis elegans embryo five somatic founder cells are born during the first cleavages. The first of these founder cells, named AB, gives rise to 389 of the 558 nuclei present in the hatching larva. Very few genes directly involved in the specification of the AB lineage have been identified so far. Here we describe a screen of a large collection of maternal-effect embryonic lethal mutations for their effect on the early expression of a pes-1::lacZ fusion gene. This fusion gene is expressed in a characteristic pattern in 14 of the 32 AB descendants present shortly after the initiation of gastrulation. Of the 37 mutations in 36 genes suspected to be required specifically during development, 12 alter the expression of the pes-1::lacZ marker construct. The gene expression pattern alterations are of four types: reduction of expression, variable expression, ectopic expression in addition to the normal pattern, and reduction of the normal pattern together with ectopic expression. We estimate that ∼100 maternal functions are required to establish the pes-1 expression pattern in the early embryo.


2017 ◽  
Vol 28 (26) ◽  
pp. 3857-3869 ◽  
Author(s):  
Kyoko Chiba ◽  
Ko-yi Chien ◽  
Yuriko Sobu ◽  
Saori Hata ◽  
Shun Kato ◽  
...  

In neurons, amyloid β-protein precursor (APP) is transported by binding to kinesin-1, mediated by JNK-interacting protein 1b (JIP1b), which generates the enhanced fast velocity (EFV) and efficient high frequency (EHF) of APP anterograde transport. Previously, we showed that EFV requires conventional interaction between the JIP1b C-terminal region and the kinesin light chain 1 (KLC1) tetratricopeptide repeat, whereas EHF requires a novel interaction between the central region of JIP1b and the coiled-coil domain of KLC1. We found that phosphorylatable Thr466 of KLC1 regulates the conventional interaction with JIP1b. Substitution of Glu for Thr466 abolished this interaction and EFV, but did not impair the novel interaction responsible for EHF. Phosphorylation of KLC1 at Thr466 increased in aged brains, and JIP1 binding to kinesin-1 decreased, suggesting that APP transport is impaired by aging. We conclude that phosphorylation of KLC1 at Thr466 regulates the velocity of transport of APP by kinesin-1 by modulating its interaction with JIP1b.


Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2842
Author(s):  
Seong-Jae Lee ◽  
Kyoung-Min Choi ◽  
Geul Bang ◽  
Seo-Gyu Park ◽  
Eun-Bi Kim ◽  
...  

Breast cancer is one of the most common malignant diseases worldwide. Astrocyte elevated gene-1 (AEG-1) is upregulated in breast cancer and regulates breast cancer cell proliferation and invasion. However, the molecular mechanisms by which AEG-1 promotes breast cancer have yet to be fully elucidated. In order to delineate the function of AEG-1 in breast cancer development, we mapped the AEG-1 interactome via affinity purification followed by LC-MS/MS. We identified nucleolin (NCL) as a novel AEG-1 interacting protein, and co-immunoprecipitation experiments validated the interaction between AEG-1 and NCL in breast cancer cells. The silencing of NCL markedly reduced not only migration/invasion, but also the proliferation induced by the ectopic expression of AEG-1. Further, we found that the ectopic expression of AEG-1 induced the tyrosine phosphorylation of c-Met, and NCL knockdown markedly reduced this AEG-1 mediated phosphorylation. Taken together, our report identifies NCL as a novel mediator of the oncogenic function of AEG-1, and suggests that c-Met could be associated with the oncogenic function of the AEG-1-NCL complex in the context of breast cancer.


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