scholarly journals Plastid-Localized EMB2726 Is Involved in Chloroplast Biogenesis and Early Embryo Development in Arabidopsis

2021 ◽  
Vol 12 ◽  
Author(s):  
Chuanling Li ◽  
Jian-Xiu Shang ◽  
Chenlei Qiu ◽  
Baowen Zhang ◽  
Jinxue Wang ◽  
...  
Keyword(s):  
Chloroplast Development ◽  
Developmental Process ◽  
Higher Plants ◽  
Critical Role ◽  
Elongation Factor ◽  
Early Embryo ◽  
The Body ◽  
Insertion Mutant ◽  
Cell Stage ◽  
Dna Insertion

Embryogenesis is a critical developmental process that establishes the body organization of higher plants. During this process, the biogenesis of chloroplasts from proplastids is essential. A failure in chloroplast development during embryogenesis can cause morphologically abnormal embryos or embryonic lethality. In this study, we isolated a T-DNA insertion mutant of the Arabidopsis gene EMBRYO DEFECTIVE 2726 (EMB2726). Heterozygous emb2726 seedlings produced about 25% albino seeds with embryos that displayed defects at the 32-cell stage and that arrested development at the late globular stage. EMB2726 protein was localized in chloroplasts and was expressed at all stages of development, such as embryogenesis. Moreover, the two translation elongation factor Ts domains within the protein were critical for its function. Transmission electron microscopy revealed that the cells in emb2726 embryos contained undifferentiated proplastids and that the expression of plastid genome-encoded photosynthesis-related genes was dramatically reduced. Expression studies of DR5:GFP, pDRN:DRN-GFP, and pPIN1:PIN1-GFP reporter lines indicated normal auxin biosynthesis but altered polar auxin transport. The expression of pSHR:SHR-GFP and pSCR:SCR-GFP confirmed that procambium and ground tissue precursors were lacking in emb2726 embryos. The results suggest that EMB2726 plays a critical role during Arabidopsis embryogenesis by affecting chloroplast development, possibly by affecting the translation process in plastids.

scholarly journals A unique AtSar1D-AtRabD2a nexus modulates autophagosome biogenesis in Arabidopsis thaliana

2021 ◽  
Vol 118 (17) ◽  
pp. e2021293118
Author(s):  
Yonglun Zeng ◽  
Baiying Li ◽  
Changyang Ji ◽  
Lei Feng ◽  
Fangfang Niu ◽  
...  
Keyword(s):  
Stress Responses ◽  
Higher Plants ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Secretory Proteins ◽  
Insertion Mutant ◽  
Intermediate Metabolites ◽  
Dna Insertion ◽  
Autophagy Pathway ◽  
Copii Vesicles

In eukaryotes, secretory proteins traffic from the endoplasmic reticulum (ER) to the Golgi apparatus via coat protein complex II (COPII) vesicles. Intriguingly, during nutrient starvation, the COPII machinery acts constructively as a membrane source for autophagosomes during autophagy to maintain cellular homeostasis by recycling intermediate metabolites. In higher plants, essential roles of autophagy have been implicated in plant development and stress responses. Nonetheless, the membrane sources of autophagosomes, especially the participation of the COPII machinery in the autophagic pathway and autophagosome biogenesis, remains elusive in plants. Here, we provided evidence in support of a novel role of a specific Sar1 homolog AtSar1d in plant autophagy in concert with a unique Rab1/Ypt1 homolog AtRabD2a. First, proteomic analysis of the plant ATG (autophagy-related gene) interactome uncovered the mechanistic connections between ATG machinery and specific COPII components including AtSar1d and Sec23s, while a dominant negative mutant of AtSar1d exhibited distinct inhibition on YFP-ATG8 vacuolar degradation upon autophagic induction. Second, a transfer DNA insertion mutant of AtSar1d displayed starvation-related phenotypes. Third, AtSar1d regulated autophagosome progression through specific recognition of ATG8e by a noncanonical motif. Fourth, we demonstrated that a plant-unique Rab1/Ypt1 homolog AtRabD2a coordinates with AtSar1d to function as the molecular switch in mediating the COPII functions in the autophagy pathway. AtRabD2a appears to be essential for bridging the specific AtSar1d-positive COPII vesicles to the autophagy initiation complex and therefore contributes to autophagosome formation in plants. Taken together, we identified a plant-specific nexus of AtSar1d-AtRabD2a in regulating autophagosome biogenesis.

scholarly journals OsASN1 Plays a Critical Role in Asparagine-Dependent Rice Development

2018 ◽  
Vol 20 (1) ◽  
pp. 130 ◽  
Author(s):  
Le Luo ◽  
Ruyi Qin ◽  
Tao Liu ◽  
Ming Yu ◽  
Tingwen Yang ◽  
...  
Keyword(s):  
Critical Role ◽  
Tiller Number ◽  
Insertion Mutant ◽  
Wild Type ◽  
Long Distance ◽  
Long Distance Transport ◽  
Similar Phenotype ◽  
Dna Insertion ◽  
Mutant Lines ◽  
Distance Transport

Asparagine is one of the important amino acids for long-distance transport of nitrogen (N) in plants. However, little is known about the effect of asparagine on plant development, especially in crops. Here, a new T-DNA insertion mutant, asparagine synthetase 1 (asn1), was isolated and showed a different plant height, root length, and tiller number compared with wild type (WT). In asn1, the amount of asparagine decreased sharply while the total nitrogen (N) absorption was not influenced. In later stages, asn1 showed reduced tiller number, which resulted in suppressed tiller bud outgrowth. The relative expression of many genes involved in the asparagine metabolic pathways declined in accordance with the decreased amino acid concentration. The CRISPR/Cas9 mutant lines of OsASN1 showed similar phenotype with asn1. These results suggest that OsASN1 is involved in the regulation of rice development and is specific for tiller outgrowth.

scholarly journals Gibberellin 20-Oxidase Gene OsGA20ox3 Regulates Plant Stature and Disease Development in Rice

2013 ◽  
Vol 26 (2) ◽  
pp. 227-239 ◽  
Author(s):  
Xue Qin ◽  
Jun Hua Liu ◽  
Wen Sheng Zhao ◽  
Xu Jun Chen ◽  
Ze Jian Guo ◽  
...  
Keyword(s):  
Transgenic Plants ◽  
Critical Role ◽  
Insertion Site ◽  
Insertion Mutant ◽  
Wild Type Plant ◽  
Wild Type ◽  
Oxidase Gene ◽  
Dna Insertion ◽  
Flanking Sequences ◽  
Plant Stature

Gibberellin (GA) 20-oxidase (GA20ox) catalyses consecutive steps of oxidation in the late part of the GA biosynthetic pathway. A T-DNA insertion mutant (17S-14) in rice, with an elongated phenotype, was isolated. Analysis of the flanking sequences of the T-DNA insertion site revealed that an incomplete T-DNA integration resulted in enhanced constitutively expression of downstream OsGA20ox3 in the mutant. The accumulation of bioactive GA1 and GA4 were increased in the mutant in comparison with the wild-type plant. Transgenic plants overexpressing OsGA20ox3 showed phenotypes similar to those of the 17S-14 mutant, and the RNA interference (RNAi) lines that had decreased OsGA20ox3 expression exhibited a semidwarf phenotype. Expression of OsGA20ox3 was detected in the leaves and roots of young seedlings, immature panicles, anthers, and pollens, based on β-glucuronidase (GUS) activity staining in transgenic plants expressing the OsGA20ox3 promoter fused to the GUS gene. The OsGA20ox3 RNAi lines showed enhanced resistance against rice pathogens Magnaporthe oryzae (causing rice blast) and Xanthomonas oryzae pv. oryzae (causing bacterial blight) and increased expression of defense-related genes. Conversely, OsGA20ox3-overexpressing plants were more susceptible to these pathogens comparing with the wild-type plants. The susceptibility of wild-type plants to X. oryzae pv. oryzae was increased by exogenous application of GA3 and decreased by S-3307 treatment. Together, the results provide direct evidence for a critical role of OsGA20ox3 in regulating not only plant stature but also disease resistance in rice.

scholarly journals Arabidopsis Seedling Lethal 1 Interacting With Plastid-Encoded RNA Polymerase Complex Proteins Is Essential for Chloroplast Development

2020 ◽  
Vol 11 ◽  
Author(s):  
Deyuan Jiang ◽  
Renjie Tang ◽  
Yafei Shi ◽  
Xiangsheng Ke ◽  
Yetao Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Chloroplast Development ◽  
Insertion Mutant ◽  
Chloroplast Gene Expression ◽  
Plant Chloroplast ◽  
Dna Insertion ◽  
Chloroplast Stroma ◽  
Underlying Mechanisms

Mitochondrial transcription termination factors (mTERFs) are highly conserved proteins in metazoans. Plants have many more mTERF proteins than animals. The functions and the underlying mechanisms of plants’ mTERFs remain largely unknown. In plants, mTERF family proteins are present in both mitochondria and plastids and are involved in gene expression in these organelles through different mechanisms. In this study, we screened Arabidopsis mutants with pigment-defective phenotypes and isolated a T-DNA insertion mutant exhibiting seedling-lethal and albino phenotypes [seedling lethal 1 (sl1)]. The SL1 gene encodes an mTERF protein localized in the chloroplast stroma. The sl1 mutant showed severe defects in chloroplast development, photosystem assembly, and the accumulation of photosynthetic proteins. Furthermore, the transcript levels of some plastid-encoded proteins were significantly reduced in the mutant, suggesting that SL1/mTERF3 may function in the chloroplast gene expression. Indeed, SL1/mTERF3 interacted with PAP12/PTAC7, PAP5/PTAC12, and PAP7/PTAC14 in the subgroup of DNA/RNA metabolism in the plastid-encoded RNA polymerase (PEP) complex. Taken together, the characterization of the plant chloroplast mTERF protein, SL1/mTERF3, that associated with PEP complex proteins provided new insights into RNA transcription in the chloroplast.

Updating long-held assumptions about fat stigma: For women, body shape plays a critical role

2020 ◽  
Author(s):  
Jaimie Krems ◽  
Steven L. Neuberg
Keyword(s):  
Body Shape ◽  
Critical Role ◽  
The Body ◽  
Theoretical Assumption ◽  
Obesity Stigma ◽  
Obese Female ◽  
Three Samples ◽  
Female Bodies ◽  
Different Parts ◽  
Fat Stigma

Heavier bodies—particularly female bodies—are stigmatized. Such fat stigma is pervasive, painful to experience, and may even facilitate weight gain, thereby perpetuating the obesity-stigma cycle. Leveraging research on functionally distinct forms of fat (deposited on different parts of the body), we propose that body shape plays an important but largely underappreciated role in fat stigma, above and beyond fat amount. Across three samples varying in participant ethnicity (White and Black Americans) and nation (U.S., India), patterns of fat stigma reveal that, as hypothesized, participants differently stigmatized equally-overweight or -obese female targets as a function of target shape, sometimes even more strongly stigmatizing targets with less rather than more body mass. Such findings suggest value in updating our understanding of fat stigma to include body shape and in querying a predominating, but often implicit, theoretical assumption that people simply view all fat as bad (and more fat as worse).

scholarly journals PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases

2021 ◽  
Vol 22 (15) ◽  
pp. 8298
Author(s):  
Hugo Christian Monroy-Ramirez ◽  
Marina Galicia-Moreno ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Arturo Santos ◽  
...  
Keyword(s):  
Liver Diseases ◽  
Metabolic Regulation ◽  
Structural Changes ◽  
Critical Role ◽  
The Body ◽  
Molecular Characteristics ◽  
Signal Pathways ◽  
Virus Infections ◽  
Physiological Processes ◽  
Hepatic Level

Carbohydrates and lipids are two components of the diet that provide the necessary energy to carry out various physiological processes to help maintain homeostasis in the body. However, when the metabolism of both biomolecules is altered, development of various liver diseases takes place; such as metabolic-associated fatty liver diseases (MAFLD), hepatitis B and C virus infections, alcoholic liver disease (ALD), and in more severe cases, hepatocelular carcinoma (HCC). On the other hand, PPARs are a family of ligand-dependent transcription factors with an important role in the regulation of metabolic processes to hepatic level as well as in other organs. After interaction with specific ligands, PPARs are translocated to the nucleus, undergoing structural changes to regulate gene transcription involved in lipid metabolism, adipogenesis, inflammation and metabolic homeostasis. This review aims to provide updated data about PPARs’ critical role in liver metabolic regulation, and their involvement triggering the genesis of several liver diseases. Information is provided about their molecular characteristics, cell signal pathways, and the main pharmacological therapies that modulate their function, currently engaged in the clinic scenario, or in pharmacological development.

scholarly journals LIN28 coordinately promotes nucleolar/ribosomal functions and represses the 2C-like transcriptional program in pluripotent stem cells

2021 ◽  
Author(s):  
Zhen Sun ◽  
Hua Yu ◽  
Jing Zhao ◽  
Tianyu Tan ◽  
Hongru Pan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryo Development ◽  
Pluripotent Stem Cells ◽  
Rna Binding ◽  
Stem Cell Differentiation ◽  
Early Embryo ◽  
Transcriptional Program ◽  
Cell Stage ◽  
Early Embryo Development ◽  
Nucleolar Stress

AbstractLIN28 is an RNA binding protein with important roles in early embryo development, stem cell differentiation/reprogramming, tumorigenesis and metabolism. Previous studies have focused mainly on its role in the cytosol where it interacts with Let-7 microRNA precursors or mRNAs, and few have addressed LIN28’s role within the nucleus. Here, we show that LIN28 displays dynamic temporal and spatial expression during murine embryo development. Maternal LIN28 expression drops upon exit from the 2-cell stage, and zygotic LIN28 protein is induced at the forming nucleolus during 4-cell to blastocyst stage development, to become dominantly expressed in the cytosol after implantation. In cultured pluripotent stem cells (PSCs), loss of LIN28 led to nucleolar stress and activation of a 2-cell/4-cell-like transcriptional program characterized by the expression of endogenous retrovirus genes. Mechanistically, LIN28 binds to small nucleolar RNAs and rRNA to maintain nucleolar integrity, and its loss leads to nucleolar phase separation defects, ribosomal stress and activation of P53 which in turn binds to and activates 2C transcription factor Dux. LIN28 also resides in a complex containing the nucleolar factor Nucleolin (NCL) and the transcriptional repressor TRIM28, and LIN28 loss leads to reduced occupancy of the NCL/TRIM28 complex on the Dux and rDNA loci, and thus de-repressed Dux and reduced rRNA expression. Lin28 knockout cells with nucleolar stress are more likely to assume a slowly cycling, translationally inert and anabolically inactive state, which is a part of previously unappreciated 2C-like transcriptional program. These findings elucidate novel roles for nucleolar LIN28 in PSCs, and a new mechanism linking 2C program and nucleolar functions in PSCs and early embryo development.

Neuronal Sodium Leak Channel Is Responsible for the Detection of Sodium in the Rat Median Preoptic Nucleus

2011 ◽  
Vol 105 (2) ◽  
pp. 650-660 ◽  
Author(s):  
Christina Tremblay ◽  
Emmanuelle Berret ◽  
Mélaine Henry ◽  
Benjamin Nehmé ◽  
Louis Nadeau ◽  
...  
Keyword(s):  
Close Contact ◽  
Critical Role ◽  
Reversal Potential ◽  
Outward Current ◽  
The Body ◽  
Equilibrium Potential ◽  
Preoptic Nucleus ◽  
Leak Channel ◽  
Median Preoptic Nucleus ◽  
Electrophysiological Recordings

Sodium (Na+) ions are of primary importance for hydromineral and cardiovascular homeostasis, and the level of Na+ in the body fluid compartments [plasma and cerebrospinal fluid (CSF)] is precisely monitored in the hypothalamus. Glial cells seem to play a critical role in the mechanism of Na+ detection. However, the precise role of neurons in the detection of extracellular Na+ concentration ([Na+]out) remains unclear. Here we demonstrate that neurons of the median preoptic nucleus (MnPO), a structure in close contact with the CSF, are specific Na+ sensors. Electrophysiological recordings were performed on dissociated rat MnPO neurons under isotonic [Na+] (100 mM NaCl) with local application of hypernatriuric (150, 180 mM NaCl) or hyponatriuric (50 mM NaCl) external solution. The hyper- and hyponatriuric conditions triggered an in- and an outward current, respectively. The reversal potential of the current matched the equilibrium potential of Na+, indicating that a change in [Na+]out modified the influx of Na+ in the MnPO neurons. The conductance of the Na+ current was not affected by either the membrane potential or the [Na+]out. Moreover, the channel was highly selective for lithium over guanidinium. Together, these data identified the channel as a Na+ leak channel. A high correlation between the electrophysiological recordings and immunofluorescent labeling for the NaX channel in dissociated MnPO neurons strongly supports this channel as a candidate for the Na+ leak channel responsible for the Na+-sensing ability of rat MnPO neurons. The absence of NaX labeling and of a specific current evoked by a change in [Na+]out in mouse MnPO neurons suggests species specificity in the hypothalamus structures participating in central Na+ detection.

scholarly journals Diesel Exhaust Particle Exposure Compromises Alveolar Macrophage Mitochondrial Bioenergetics

2019 ◽  
Vol 20 (22) ◽  
pp. 5598
Author(s):  
Jonathan L. Gibbs ◽  
Blake W. Dallon ◽  
Joshua B. Lewis ◽  
Chase M. Walton ◽  
Juan A. Arroyo ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Diesel Exhaust ◽  
Critical Role ◽  
Cell Communication ◽  
Diesel Exhaust Particle ◽  
Diesel Exhaust Particles ◽  
The Body ◽  
Whole Body ◽  
H2o2 Production ◽  
Pulmonary Macrophages

Diesel exhaust particles (DEPs) are known pathogenic pollutants that constitute a significant quantity of air pollution. Given the ubiquitous presence of macrophages throughout the body, including the lungs, as well as their critical role in tissue and organismal metabolic function, we sought to determine the effect of DEP exposure on macrophage mitochondrial function. Following daily DEP exposure in mice, pulmonary macrophages were isolated for mitochondrial analyses, revealing reduced respiration rates and dramatically elevated H2O2 levels. Serum ceramides and inflammatory cytokines were increased. To determine the degree to which the changes in mitochondrial function in macrophages were not dependent on any cross-cell communication, primary pulmonary murine macrophages were used to replicate the DEP exposure in a cell culture model. We observed similar changes as seen in pulmonary macrophages, namely diminished mitochondrial respiration, but increased H2O2 production. Interestingly, when treated with myriocin to inhibit ceramide biosynthesis, these DEP-induced mitochondrial changes were mitigated. Altogether, these data suggest that DEP exposure may compromise macrophage mitochondrial and whole-body function via pathologic alterations in macrophage ceramide metabolism.

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