scholarly journals Metabolite Profiling in Arabidopsis thaliana with Moderately Impaired Photorespiration Reveals Novel Metabolic Links and Compensatory Mechanisms of Photorespiration

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 391
Author(s):  
Stefan Timm ◽  
Adriano Nunes-Nesi ◽  
Alexandra Florian ◽  
Marion Eisenhut ◽  
Katja Morgenthal ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Isotope Labeling ◽  
Sulfur Metabolism ◽  
Primary Metabolism ◽  
Metabolome Analysis ◽  
Compensatory Mechanisms ◽  
Glycerate Kinase ◽  
Hydroxypyruvate Reductase ◽  
Cellular Processes ◽  
Underlying Mechanisms

Photorespiration is an integral component of plant primary metabolism. Accordingly, it has been often observed that impairing the photorespiratory flux negatively impacts other cellular processes. In this study, the metabolic acclimation of the Arabidopsis thaliana wild type was compared with the hydroxypyruvate reductase 1 (HPR1; hpr1) mutant, displaying only a moderately reduced photorespiratory flux. Plants were analyzed during development and under varying photoperiods with a combination of non-targeted and targeted metabolome analysis, as well as 13C- and 14C-labeling approaches. The results showed that HPR1 deficiency is more critical for photorespiration during the vegetative compared to the regenerative growth phase. A shorter photoperiod seems to slowdown the photorespiratory metabolite conversion mostly at the glycerate kinase and glycine decarboxylase steps compared to long days. It is demonstrated that even a moderate impairment of photorespiration severely reduces the leaf-carbohydrate status and impacts on sulfur metabolism. Isotope labeling approaches revealed an increased CO2 release from hpr1 leaves, most likely occurring from enhanced non-enzymatic 3-hydroxypyruvate decarboxylation and a higher flux from serine towards ethanolamine through serine decarboxylase. Collectively, the study provides evidence that the moderate hpr1 mutant is an excellent tool to unravel the underlying mechanisms governing the regulation of metabolic linkages of photorespiration with plant primary metabolism.

scholarly journals Brassinosteroids repress the seed maturation program during the seed-to-seedling transition

2021 ◽  
Author(s):  
Jiuxiao Ruan ◽  
Huhui Chen ◽  
Tao Zhu ◽  
Yaoguang Yu ◽  
Yawen Lei ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Abscisic Acid ◽  
Plant Hormone ◽  
Flowering Plants ◽  
Seed Maturation ◽  
Domain Protein ◽  
Abscisic Acid Insensitive3 ◽  
Underlying Mechanisms ◽  
Embryonic Structure

Abstract In flowering plants, repression of the seed maturation program is essential for the transition from the seed to the vegetative phase, but the underlying mechanisms remain poorly understood. The B3-domain protein VIVIPAROUS1/ABSCISIC ACID-INSENSITIVE3-LIKE 1 (VAL1) is involved in repressing the seed maturation program. Here we uncovered a molecular network triggered by the plant hormone brassinosteroid (BR) that inhibits the seed maturation program during the seed-to-seedling transition in Arabidopsis (Arabidopsis thaliana). val1-2 mutant seedlings treated with a BR biosynthesis inhibitor form embryonic structures, whereas BR signaling gain-of-function mutations rescue the embryonic structure trait. Furthermore, the BR-activated transcription factors BRI1-EMS-SUPPRESSOR 1 and BRASSINAZOLE-RESISTANT 1 bind directly to the promoter of AGAMOUS-LIKE15 (AGL15), which encodes a transcription factor involved in activating the seed maturation program, and suppress its expression. Genetic analysis indicated that BR signaling is epistatic to AGL15 and represses the seed maturation program by downregulating AGL15. Finally, we showed that the BR-mediated pathway functions synergistically with the VAL1/2-mediated pathway to ensure the full repression of the seed maturation program. Together, our work uncovered a mechanism underlying the suppression of the seed maturation program, shedding light on how BR promotes seedling growth.

SNF1-related protein kinase 1: the many-faced signaling hub regulating developmental plasticity in plants

2021 ◽  
Author(s):  
Muhammed Jamsheer K ◽  
Manoj Kumar ◽  
Vibha Srivastava
Keyword(s):  
Protein Kinase ◽  
Environmental Conditions ◽  
Protein Trafficking ◽  
Developmental Plasticity ◽  
Inositol Phosphate ◽  
Future Research ◽  
Primary Metabolism ◽  
Related Protein ◽  
Comprehensive Overview ◽  
Cellular Processes

AbstractThe Snf1-related protein kinase 1 (SnRK1) is the plant homolog of the heterotrimeric AMP-activated protein kinase/sucrose non-fermenting 1 (AMPK/Snf1), which works as a major regulator of growth under nutrient-limiting conditions in eukaryotes. Along with its conserved role as a master regulator of sugar starvation responses, SnRK1 is involved in controlling the developmental plasticity and resilience under diverse environmental conditions in plants. In this review, through mining and analyzing the interactome and phosphoproteome data of SnRK1, we are highlighting its role in fundamental cellular processes such as gene regulation, protein synthesis, primary metabolism, protein trafficking, nutrient homeostasis, and autophagy. Along with the well-characterized molecular interaction in SnRK1 signaling, our analysis highlights several unchartered regions of SnRK1 signaling in plants such as its possible communication with chromatin remodelers, histone modifiers, and inositol phosphate signaling. We also discuss potential reciprocal interactions of SnRK1 signaling with other signaling pathways and cellular processes, which could be involved in maintaining flexibility and homeostasis under different environmental conditions. Overall, this review provides a comprehensive overview of the SnRK1 signaling network in plants and suggests many novel directions for future research.

scholarly journals MiRNA-143 mediates the proliferative signaling pathway of FSH and regulates estradiol production

2017 ◽  
Vol 234 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Li Zhang ◽  
XiaoXin Zhang ◽  
Xuejing Zhang ◽  
Yu Lu ◽  
Lei Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Loss Of Function ◽  
Cellular Processes ◽  
Cell Functions ◽  
Genes Expression ◽  
Underlying Mechanisms

MicroRNAs (MiRNAs) play important regulatory roles in many cellular processes. MiR-143 is highly enriched in the mouse ovary, but its roles and underlying mechanisms are not well understood. In the current study, we show that miR-143 is located in granulosa cells of primary, secondary and antral follicles. To explore the specific functions of miR-143, we transfected miR-143 inhibitor into primary cultured granulosa cells to study the loss of function of miR-143 and the results showed that miR-143 silencing significantly increased estradiol production and steroidogenesis-related gene expression. Moreover, our in vivo and in vitro studies showed that follicular stimulating hormone (FSH) significantly decreased miR-143 expression. This function of miR-143 is accomplished by its binding to the 3’-UTR of KRAS mRNA. Furthermore, our results demonstrated that miR-143 acts as a negative regulating molecule mediating the signaling pathway of FSH and affecting estradiol production by targeting KRAS. MiR-143 also negatively acts in regulating granulosa cells proliferation and cell cycle-related genes expression. These findings indicate that miR-143 plays vital roles in FSH-induced estradiol production and granulosa cell proliferation, providing a novel mechanism that involves miRNA in regulating granulosa cell functions.

scholarly journals Lipocalin 2 as Putative Modulator of Local Inflammatory Processes in the Spinal Cord and Component of Organ Cross-talk After Spinal Cord Injury

2021 ◽  
Author(s):  
Victoria Behrens ◽  
Clara Voelz ◽  
Nina Müller ◽  
Weiyi Zhao ◽  
Tim Clarner ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Serum ◽  
Negative Influence ◽  
Lipocalin 2 ◽  
Cellular Processes ◽  
Cord Injury ◽  
Inflammatory Processes ◽  
Underlying Mechanisms ◽  
Sites Of Action

Abstract Lipocalin 2 (Lcn2), an immunomodulator, regulates various cellular processes such as iron transport and defense against bacterial infection. Under pathological conditions, Lcn2 promotes neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes. Although it seems to have a negative influence on the functional outcome in spinal cord injury (SCI), the extent of its involvement in SCI and the underlying mechanisms are not yet fully known. In this study, using a SCI contusion mouse model, we first investigated the expression pattern of Lcn2 in different parts of the CNS (spinal cord and brain), blood serum and in the liver. Interestingly, we could note a significant increase in Lcn2 throughout the whole spinal cord, in the brain, liver and in blood serum. This demonstrates the diversity of its possible sites of action in SCI. Further, genetic deficiency of Lcn2 (Lcn2-/-) significantly reduced certain aspects of gliosis in the SCI-mice. Taken together, our studies provide first valuable hints, suggesting that Lcn2 is involved in the local and systemic effects post SCI, and might modulate the impairment of different peripheral organs after injury.

scholarly journals Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau

2020 ◽  
Vol 46 (1) ◽  
pp. 98-115 ◽  
Author(s):  
Sruti Rayaprolu ◽  
Lenora Higginbotham ◽  
Pritha Bagchi ◽  
Caroline M. Watson ◽  
Tian Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Network ◽  
Protein Biomarkers ◽  
Cellular Processes ◽  
Complex Protein ◽  
Underlying Mechanisms ◽  
Novel Protein

AbstractThe repeated failures of amyloid-targeting therapies have challenged our narrow understanding of Alzheimer’s disease (AD) pathogenesis and inspired wide-ranging investigations into the underlying mechanisms of disease. Increasing evidence indicates that AD develops from an intricate web of biochemical and cellular processes that extend far beyond amyloid and tau accumulation. This growing recognition surrounding the diversity of AD pathophysiology underscores the need for holistic systems-based approaches to explore AD pathogenesis. Here we describe how network-based proteomics has emerged as a powerful tool and how its application to the AD brain has provided an informative framework for the complex protein pathophysiology underlying the disease. Furthermore, we outline how the AD brain network proteome can be leveraged to advance additional scientific and translational efforts, including the discovery of novel protein biomarkers of disease.

scholarly journals What Role Does CFTR Play in Development, Differentiation, Regeneration and Cancer?

2020 ◽  
Vol 21 (9) ◽  
pp. 3133 ◽  
Author(s):  
Margarida D. Amaral ◽  
Margarida C. Quaresma ◽  
Ines Pankonien
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Mesenchymal Transition ◽  
Transmembrane Conductance Regulator ◽  
Foetal Development ◽  
Term Survival ◽  
Mesenchymal Transition ◽  
Cellular Processes ◽  
Underlying Mechanisms ◽  
Novel Therapeutic Strategies ◽  
Open Question

One of the key features associated with the substantial increase in life expectancy for individuals with CF is an elevated predisposition to cancer, firmly established by recent studies involving large cohorts. With the recent advances in cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies and the increased long-term survival rate of individuals with cystic fibrosis (CF), this is a novel challenge emerging at the forefront of this disease. However, the mechanisms linking dysfunctional CFTR to carcinogenesis have yet to be unravelled. Clues to this challenging open question emerge from key findings in an increasing number of studies showing that CFTR plays a role in fundamental cellular processes such as foetal development, epithelial differentiation/polarization, and regeneration, as well as in epithelial–mesenchymal transition (EMT). Here, we provide state-of-the-art descriptions on the moonlight roles of CFTR in these processes, highlighting how they can contribute to novel therapeutic strategies. However, such roles are still largely unknown, so we need rapid progress in the elucidation of the underlying mechanisms to find the answers and thus tailor the most appropriate therapeutic approaches.

scholarly journals Biogenesis of the Spacious Coxiella-Containing Vacuole Depends on Host Transcription Factors TFEB and TFE3

2019 ◽  
Vol 88 (3) ◽  
Author(s):  
Bhavna Padmanabhan ◽  
Laura F. Fielden ◽  
Abderrahman Hachani ◽  
Patrice Newton ◽  
David R. Thomas ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Host Cell ◽  
Isotope Labeling ◽  
Nuclear Translocation ◽  
Bacterial Pathogen ◽  
Effector Proteins ◽  
Content Type ◽  
Cellular Processes ◽  
Type Iv ◽  
Lysosome Biogenesis

ABSTRACT Coxiella burnetii is an obligate intracellular bacterial pathogen that replicates inside the lysosome-derived Coxiella-containing vacuole (CCV). To establish this unique niche, C. burnetii requires the Dot/Icm type IV secretion system (T4SS) to translocate a cohort of effector proteins into the host cell, which modulate multiple cellular processes. To characterize the host-pathogen interactions that occur during C. burnetii infection, stable-isotope labeling by amino acids in cell culture (SILAC)-based proteomics was used to identify changes in the host proteome during infection of a human-derived macrophage cell line. These data revealed that the abundances of many proteins involved in host cell autophagy and lysosome biogenesis were increased in infected cells. Thus, the role of the host transcription factors TFEB and TFE3, which regulate the expression of a network of genes involved in autophagy and lysosomal biogenesis, were examined in the context of C. burnetii infection. During infection with C. burnetii, both TFEB and TFE3 were activated, as demonstrated by the transport of these proteins from the cytoplasm into the nucleus. The nuclear translocation of these transcription factors was shown to be dependent on the T4SS, as a Dot/Icm mutant showed reduced nuclear translocation of TFEB and TFE3. This was supported by the observation that blocking bacterial translation with chloramphenicol resulted in the movement of TFEB and TFE3 back into the cytoplasm. Silencing of the TFEB and TFE3 genes, alone or in combination, significantly reduced the size of the CCV, which indicates that these host transcription factors facilitate the expansion and maintenance of the organelle that supports C. burnetii intracellular replication.

scholarly journals Perturbations in the Primary Metabolism of Tomato and Arabidopsis thaliana Plants Infected with the Soil-Borne Fungus Verticillium dahliae

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0138242 ◽  
Author(s):  
Anja Buhtz ◽  
Katja Witzel ◽  
Nadine Strehmel ◽  
Jörg Ziegler ◽  
Steffen Abel ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Verticillium Dahliae ◽  
Primary Metabolism

scholarly journals Emerging impact of the long noncoding RNA MIR22HG on proliferation and apoptosis in multiple human cancers

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Le Zhang ◽  
Cuixia Li ◽  
Xiulan Su
Keyword(s):  
Chromatin Remodeling ◽  
Noncoding Rna ◽  
Potential Role ◽  
Immune Escape ◽  
Prognostic Biomarker ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Underlying Mechanisms ◽  
Competitive Endogenous Rna

AbstractAn increasing number of studies have shown that long noncoding RNAs (lncRNAs) play important roles in diverse cellular processes, including proliferation, apoptosis, migration, invasion, chromatin remodeling, metabolism and immune escape. Clinically, the expression of MIR22HG is increased in many human tumors (colorectal cancer, gastric cancer, hepatocellular carcinoma, lung cancer, and thyroid carcinoma), while in others (esophageal adenocarcinoma and glioblastoma), it is significantly decreased. Moreover, MIR22HG has been reported to function as a competitive endogenous RNA (ceRNA), be involved in signaling pathways, interact with proteins and interplay with miRNAs as a host gene to participate in tumorigenesis and tumor progression. In this review, we describe the biological functions of MIR22HG, reveal its underlying mechanisms for cancer regulation, and highlight the potential role of MIR22HG as a novel cancer prognostic biomarker and therapeutic target that can increase the efficacy of immunotherapy and targeted therapy for cancer treatment.

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