LAZY1 Controls Tiller Angle and Shoot Gravitropism by Regulating the Expression of Auxin Transporters and Signaling Factors in Rice

2020 ◽  
Author(s):  
Mo Zhu ◽  
Yanjuan Hu ◽  
Aizi Tong ◽  
Bowen Yan ◽  
Yanpeng Lv ◽  
...  
Keyword(s):  
Plant Architecture ◽  
Planting Density ◽  
Cellular Functions ◽  
Control Gene Expression ◽  
Protein Dna Interactions ◽  
Key Factor ◽  
Localization Signal ◽  
Shoot Gravitropism ◽  
Insight Into ◽  
Tiller Angle

Abstract Tiller angle is a key factor determining rice plant architecture, planting density, light interception, photosynthetic efficiency, disease resistance, and grain yield. However, the mechanisms underlying tiller angle control are far from clear. In this study, we identified a mutant, termed bta1–1, with an enlarged tiller angle throughout its life cycle. A detailed analysis reveals that BTA1 has multiple functions because tiller angle, shoot gravitropism, and tolerance to drought stress are changed in bta1–1 plants. Moreover, BTA1 is a positive regulator of shoot gravitropism in rice. Shoot responses to gravistimulation are disrupted in bta1-1 under both light and dark conditions. Gene cloning reveals that bta1-1 is a novel mutant allele of LA1 renamed la1-SN. LA1 is able to rescue the tiller angle and shoot gravitropism defects observed in la1-SN. The nuclear localization signal of LA1 is disrupted by la1-SN, causing changes of its subcellular localization. LA1 is required to regulate the expression of auxin transporters and signaling factors that control shoot gravitropism and tiller angle. High-throughput mRNA sequencing is performed to elucidate the molecular and cellular functions of LA1. The results show that LA1 may be involved in the nucleosome and chromatin assembly, and protein-DNA interactions to control gene expression, shoot gravitropism, and tiller angle. Our results provide new insight into the mechanisms whereby LA1 controls shoot gravitropism and tiller angle in rice.

scholarly journals Development of the PARMS marker of the TAC1 gene and its utilization in rice plant architecture breeding

Euphytica ◽  
2021 ◽  
Vol 217 (3) ◽  
Author(s):  
Ju Gao ◽  
Haifu Liang ◽  
Juan Huang ◽  
Dongjin Qing ◽  
Hao Wu ◽  
...  
Keyword(s):  
Rice Plant ◽  
Plant Architecture ◽  
Molecular Design ◽  
High Yield ◽  
Amplification Refractory Mutation System ◽  
Japonica Rice ◽  
Rice Varieties ◽  
Key Factor ◽  
Tiller Angle ◽  
The Ideal

AbstractThe ideal plant architecture is a new strategy for super high yield breeding of rice. Tiller angle is an important plant architecture character of rice. A reasonable tiller angle is a key factor for the ideal plant architecture and achieving high-yield breeding. Molecular design breeding is the most potential new direction of crop breeding in the future. The development of accurate and efficient functional molecular markers of target trait genes is crucial for molecular design breeding. The TAC1 (Tiller Angle Controlling) gene is the primary gene that regulates tiller angle in rice. This gene can be used to improve the compact plant architecture of indica and japonica rice varieties. The SNP variation from A to G at the fourth intron 3′ splicing point in TAC1 changes plant architecture. Based on the SNP variation, PM-TAC1 was successfully developed as a fluorescent functional molecular marker, via the penta-primer amplification refractory mutation system. Ninety-three rice materials were genotyped using this marker, and the marker was effectively used in rice plant architecture breeding. The successful development of this marker will contribute to the molecular breeding of rice plant architecture.

scholarly journals Disease related mutations in PI3Kγ disrupt regulatory C-terminal dynamics and reveals a path to selective inhibitors

2020 ◽  
Author(s):  
Manoj K Rathinaswamy ◽  
Zied Gaieb ◽  
Kaelin D Fleming ◽  
Chiara Borsari ◽  
Noah J Harris ◽  
...  
Keyword(s):  
Conformational Changes ◽  
Kinase Activity ◽  
Inflammatory Diseases ◽  
Selective Inhibitors ◽  
Cellular Functions ◽  
C Terminus ◽  
Key Factor ◽  
Terminal Dynamics ◽  
Therapeutic Development ◽  
Insight Into

AbstractClass I Phosphoinositide 3-kinases (PI3Ks) are master regulators of cellular functions, with the p110γ subunit playing a key role in immune signalling. PI3Kγ is a key factor in inflammatory diseases, and has been identified as a therapeutic target for cancers due to its immunomodulatory role. Using a combined biochemical/biophysical approach, we have revealed insight into regulation of kinase activity, specifically defining how immunodeficiency and oncogenic mutations of R1021 in the c-terminus can inactivate or activate enzyme activity. Screening of small molecule inhibitors using HDX-MS revealed that activation loop binding inhibitors induce allosteric conformational changes that mimic those seen for the R1021C mutant. Structural analysis of clinically advanced PI3K inhibitors revealed novel binding pockets that can be exploited for further therapeutic development. Overall this work provides unique insight into the regulatory mechanisms that control PI3Kγ kinase activity, and shows a framework for the design of PI3K isoform and mutant selective inhibitors.

scholarly journals Bone morphogenetic proteins, breast cancer, and bone metastases: striking the right balance

2017 ◽  
Vol 24 (10) ◽  
pp. R349-R366 ◽  
Author(s):  
Catherine Zabkiewicz ◽  
Jeyna Resaul ◽  
Rachel Hargest ◽  
Wen Guo Jiang ◽  
Lin Ye
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Bone Morphogenetic Proteins ◽  
Therapeutic Potential ◽  
Current Knowledge ◽  
Breast Tumour ◽  
Cellular Functions ◽  
Foetal Development ◽  
Key Factor ◽  
The Right

Bone morphogenetic proteins (BMPs) belong to the TGF-β super family, and are essential for the regulation of foetal development, tissue differentiation and homeostasis and a multitude of cellular functions. Naturally, this has led to the exploration of aberrance in this highly regulated system as a key factor in tumourigenesis. Originally identified for their role in osteogenesis and bone turnover, attention has been turned to the potential role of BMPs in tumour metastases to, and progression within, the bone niche. This is particularly pertinent to breast cancer, which commonly metastasises to bone, and in which studies have revealed aberrations of both BMP expression and signalling, which correlate clinically with breast cancer progression. Ultimately a BMP profile could provide new prognostic disease markers. As the evidence suggests a role for BMPs in regulating breast tumour cellular function, in particular interactions with tumour stroma and the bone metastatic microenvironment, there may be novel therapeutic potential in targeting BMP signalling in breast cancer. This review provides an update on the current knowledge of BMP abnormalities and their implication in the development and progression of breast cancer, particularly in the disease-specific bone metastasis.

What determines a boundary for navigating a complex street network: evidence from London taxi drivers

2021 ◽  
pp. 1-20
Author(s):  
Eva-Maria Griesbauer ◽  
Ed Manley ◽  
Daniel McNamee ◽  
Jeremy Morley ◽  
Hugo Spiers
Keyword(s):  
Urban Space ◽  
Large Scale ◽  
Route Planning ◽  
Taxi Drivers ◽  
Street Networks ◽  
Planning Models ◽  
Key Factor ◽  
Efficient Planning ◽  
Regent's Park ◽  
Insight Into

Abstract Spatial boundaries play an important role in defining spaces, structuring memory and supporting planning during navigation. Recent models of hierarchical route planning use boundaries to plan efficiently first across regions and then within regions. However, it remains unclear which structures (e.g. parks, rivers, major streets, etc.) will form salient boundaries in real-world cities. This study tested licensed London taxi drivers, who are unique in their ability to navigate London flexibly without physical navigation aids. They were asked to indicate streets they considered as boundaries for London districts or dividing areas. It was found that agreement on boundary streets varied considerably, from some boundaries providing almost no consensus to some boundaries consistently noted as boundaries. Examining the properties of the streets revealed that a key factor in the consistent boundaries was the near rectilinear nature of the designated region (e.g. Mayfair and Soho) and the distinctiveness of parks (e.g. Regent's Park). Surprisingly, the River Thames was not consistently considered as a boundary. These findings provide insight into types of environmental features that lead to the perception of explicit boundaries in large-scale urban space. Because route planning models assume that boundaries are used to segregate the space for efficient planning, these results help make predictions of the likely planning demands of different routes in such complex large-scale street networks. Such predictions could be used to highlight information used for navigation guidance applications to enable more efficient hierarchical planning and learning of large-scale environments.

scholarly journals 3D micro-environment regulates NF–κβ dependent adhesion to induce monocyte differentiation

2018 ◽  
Author(s):  
Anindita Bhattacharya ◽  
Mahesh Agarwal ◽  
Rachita Mukherjee ◽  
Prosenjit Sen ◽  
Deepak Kumar Sinha
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
The Novel ◽  
Monocyte Adhesion ◽  
Cellular Functions ◽  
Monocyte Differentiation ◽  
Summary Statement ◽  
Necessary And Sufficient ◽  
Multiple Signaling ◽  
Insight Into

AbstractDifferentiation of monocytes entails their relocation from blood to the tissue, hence accompanied by an altered physicochemical micro-environment. While the mechanism by which the biochemical make-up of the micro-environment induces differentiation is known, the fluid-like to gel-like transition in the physical micro-environment is not well understood. Monocytes maintain non-adherent state to prevent differentiation. We establish that irrespective of the chemical makeup, a 3D gel-like micro-environment induces a positive-feedback loop of adhesion-MAPK-NF-κβ activation to facilitate differentiation. In 2D fluid-like micro-environment, adhesion alone is capable of inducing differentiation via the same positive-feedback signalling. Chemical inducer treatment in fluid-like micro-environment, increases the propensity of monocyte adhesion via a brief pulse of p-MAPK. The adhesion subsequently elicit differentiation, establishing that adhesion is both necessary and sufficient to induce differentiation in 2D/3D micro-environment. Our findings challenge the notion that adhesion is a result of monocyte differentiation. Rather it’s the adhesion which triggers the differentiation of monocytes. MAPK, and NF-κβ being key molecules of multiple signaling pathways, we hypothesize that biochemically inert 3D gel-like micro-environment would also influence other cellular functions.Summary statementThis article brings out a new insight into the novel mechanisms of monocyte differentiation solely driven by physical micro-environment and adhesion.

scholarly journals C-terminal tail polyglycylation and polyglutamylation alter microtubule mechanical properties

2019 ◽  
Author(s):  
Kathryn P. Wall ◽  
Harold Hart ◽  
Thomas Lee ◽  
Cynthia Page ◽  
Taviare L. Hawkins ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Molecular Mechanisms ◽  
High Stress ◽  
Resonance Spectroscopy ◽  
Post Translational Modification ◽  
Cellular Functions ◽  
Peptide Backbone ◽  
Post Translational Modifications ◽  
Intrinsic Stiffness ◽  
Insight Into

ABSTRACTMicrotubules are biopolymers that perform diverse cellular functions. The regulation of microtubule behavior occurs in part through post-translational modification of both the α- and β- subunits of tubulin. One class of modifications is the heterogeneous addition of glycine and glutamate residues to the disordered C-terminal tails of tubulin. Due to their prevalence in stable, high stress cellular structures such as cilia, we sought to determine if these modifications alter the intrinsic stiffness of microtubules. Here we describe the purification and characterization of differentially-modified pools of tubulin from Tetrahymena thermophila. We found that glycylation on the α-C-terminal tail is a key determinant of microtubule stiffness, but does not affect the number of protofilaments incorporated into microtubules. We measured the dynamics of the tail peptide backbone using nuclear magnetic resonance spectroscopy. We found that the spin-spin relaxation rate (R2) showed a pronounced decreased as a function of distance from the tubulin surface for the α-tubulin tail, indicating that the α-tubulin tail interacts with the dimer surface. This suggests that the interactions of the α-C-terminal tail with the tubulin body contributes to the stiffness of the assembled microtubule, providing insight into the mechanism by which glycylation and glutamylation can alter microtubule mechanical properties.SIGNIFICANCEMicrotubules are regulated in part by post-translational modifications including the heterogeneous addition of glycine and glutamate residues to the C-terminal tails. By producing and characterizing differentially-modified tubulin, this work provides insight into the molecular mechanisms of how these modifications alter intrinsic microtubule properties such as flexibility. These results have broader implications for mechanisms of how ciliary structures are able to function under high stress.

scholarly journals The cytoplasmic tail of human mannosidase Man1b1 contributes to catalysis-independent quality control of misfolded alpha1-antitrypsin

2020 ◽  
Vol 117 (40) ◽  
pp. 24825-24836 ◽  
Author(s):  
Ashlee H. Sun ◽  
John R. Collette ◽  
Richard N. Sifers
Keyword(s):  
Secretory Pathway ◽  
Cytoplasmic Tail ◽  
Cellular Functions ◽  
Independent Manner ◽  
Accelerated Degradation ◽  
Naturally Occurring ◽  
Regulatory Capacity ◽  
Alpha1 Antitrypsin ◽  
Catalytic Removal ◽  
Insight Into

The failure of polypeptides to achieve conformational maturation following biosynthesis can result in the formation of protein aggregates capable of disrupting essential cellular functions. In the secretory pathway, misfolded asparagine (N)-linked glycoproteins are selectively sorted for endoplasmic reticulum-associated degradation (ERAD) in response to the catalytic removal of terminal alpha-linked mannose units. Remarkably, ER mannosidase I/Man1b1, the first alpha-mannosidase implicated in this conventional N-glycan-mediated process, can also contribute to ERAD in an unconventional, catalysis-independent manner. To interrogate this functional dichotomy, the intracellular fates of two naturally occurring misfolded N-glycosylated variants of human alpha1-antitrypsin (AAT), Null Hong Kong (NHK), and Z (ATZ), in Man1b1 knockout HEK293T cells were monitored in response to mutated or truncated forms of transfected Man1b1. As expected, the conventional catalytic system requires an intact active site in the Man1b1 luminal domain. In contrast, the unconventional system is under the control of an evolutionarily extended N-terminal cytoplasmic tail. Also, N-glycans attached to misfolded AAT are not required for accelerated degradation mediated by the unconventional system, further demonstrating its catalysis-independent nature. We also established that both systems accelerate the proteasomal degradation of NHK in metabolic pulse-chase labeling studies. Taken together, these results have identified the previously unrecognized regulatory capacity of the Man1b1 cytoplasmic tail and provided insight into the functional dichotomy of Man1b1 as a component in the mammalian proteostasis network.

scholarly journals Recent Insight into SARS-CoV2 Immunopathology and Rationale for Potential Treatment and Preventive Strategies in COVID-19

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 224 ◽  
Author(s):  
Sara Lega ◽  
Samuele Naviglio ◽  
Stefano Volpi ◽  
Alberto Tommasini
Keyword(s):  
Severe Disease ◽  
Host Immune System ◽  
Great Effort ◽  
Clinical Observations ◽  
Current State ◽  
Key Factor ◽  
Pharmacologic Treatments ◽  
Immunomodulating Drugs ◽  
Insight Into

As the outbreak of the new coronavirus (SARS-CoV-2) infection is spreading globally, great effort is being made to understand the disease pathogenesis and host factors that predispose to disease progression in an attempt to find a window of opportunity for intervention. In addition to the direct cytopathic effect of the virus, the host hyper-inflammatory response has emerged as a key factor in determining disease severity and mortality. Accumulating clinical observations raised hypotheses to explain why some patients develop more severe disease while others only manifest mild or no symptoms. So far, Covid-19 management remains mainly supportive. However, many researches are underway to clarify the role of antiviral and immunomodulating drugs in changing morbidity and mortality in patients who become severely ill. This review summarizes the current state of knowledge on the interaction between SARS-CoV-2 and the host immune system and discusses recent findings on proposed pharmacologic treatments.

Regulation of the water channel aquaporin-2 by posttranslational modification

2011 ◽  
Vol 300 (5) ◽  
pp. F1062-F1073 ◽  
Author(s):  
Hanne B. Moeller ◽  
Emma T. B. Olesen ◽  
Robert A. Fenton
Keyword(s):  
Membrane Proteins ◽  
Protein Interactions ◽  
Posttranslational Modifications ◽  
Posttranslational Modification ◽  
Water Channel ◽  
Cellular Functions ◽  
Aquaporin 2 ◽  
Eukaryotic Membrane Proteins ◽  
Insight Into

The cellular functions of many eukaryotic membrane proteins, including the vasopressin-regulated water channel aquaporin-2 (AQP2), are regulated by posttranslational modifications. In this article, we discuss the experimental discoveries that have advanced our understanding of how posttranslational modifications affect AQP2 function, especially as they relate to the role of AQP2 in the kidney. We review the most recent data demonstrating that glycosylation and, in particular, phosphorylation and ubiquitination are mechanisms that regulate AQP2 activity, subcellular sorting and distribution, degradation, and protein interactions. From a clinical perspective, posttranslational modification resulting in protein misrouting or degradation may explain certain forms of nephrogenic diabetes insipidus. In addition to providing major insight into the function and dynamics of renal AQP2 regulation, the analysis of AQP2 posttranslational modification may provide general clues as to the role of posttranslational modification for regulation of other membrane proteins.

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