scholarly journals Peptide–Oleate Complexes Create Novel Membrane-Bound Compartments

2020 ◽  
Vol 37 (11) ◽  
pp. 3083-3093
Author(s):  
Jesper S Hansen ◽  
Tuan Hiep Tran ◽  
Michele Cavalera ◽  
Sanchari Paul ◽  
Arunima Chaudhuri ◽  
...  

Abstract A challenging question in evolutionary theory is the origin of cell division and plausible molecular mechanisms involved. Here, we made the surprising observation that complexes formed by short alpha-helical peptides and oleic acid can create multiple membrane-enclosed spaces from a single lipid vesicle. The findings suggest that such complexes may contain the molecular information necessary to initiate and sustain this process. Based on these observations, we propose a new molecular model to understand protocell division.

BIOspektrum ◽  
2020 ◽  
Vol 26 (7) ◽  
pp. 739-742
Author(s):  
Anne Schlaitz

AbstractIn order to divide successfully, cells need to reorganize their interior including membrane-bound organelles such as the endoplasmic reticulum (ER). The ER serves as sink and source for the nuclear envelope and undergoes distinct transformations in its morphology and dynamics during cell division. To fully appreciate the functions of ER remodeling during cell division it will be essential to first achieve a detailed understanding of the underlying molecular mechanisms.


2014 ◽  
Vol 106 (2) ◽  
pp. 292a ◽  
Author(s):  
Erik Strandberg ◽  
Ariadna Grau-Campistany ◽  
Parvesh Wadhwani ◽  
Johannes Reichert ◽  
Jochen Bürck ◽  
...  

1999 ◽  
Vol 82 (08) ◽  
pp. 277-282 ◽  
Author(s):  
Yuri Veklich ◽  
Jean-Philippe Collet ◽  
Charles Francis ◽  
John W. Weisel

IntroductionMuch is known about the fibrinolytic system that converts fibrin-bound plasminogen to the active protease, plasmin, using plasminogen activators, such as tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator. Plasmin then cleaves fibrin at specific sites and generates soluble fragments, many of which have been characterized, providing the basis for a molecular model of the polypeptide chain degradation.1-3 Soluble degradation products of fibrin have also been characterized by transmission electron microscopy, yielding a model for their structure.4 Moreover, high resolution, three-dimensional structures of certain fibrinogen fragments has provided a wealth of information that may be useful in understanding how various proteins bind to fibrin and the overall process of fibrinolysis (Doolittle, this volume).5,6 Both the rate of fibrinolysis and the structures of soluble derivatives are determined in part by the fibrin network structure itself. Furthermore, the activation of plasminogen by t-PA is accelerated by the conversion of fibrinogen to fibrin, and this reaction is also affected by the structure of the fibrin. For example, clots made of thin fibers have a decreased rate of conversion of plasminogen to plasmin by t-PA, and they generally are lysed more slowly than clots composed of thick fibers.7-9 Under other conditions, however, clots made of thin fibers may be lysed more rapidly.10 In addition, fibrin clots composed of abnormally thin fibers formed from certain dysfibrinogens display decreased plasminogen binding and a lower rate of fibrinolysis.11-13 Therefore, our increasing knowledge of various dysfibrinogenemias will aid our understanding of mechanisms of fibrinolysis (Matsuda, this volume).14,15 To account for these diverse observations and more fully understand the molecular basis of fibrinolysis, more knowledge of the physical changes in the fibrin matrix that precede solubilization is required. In this report, we summarize recent experiments utilizing transmission and scanning electron microscopy and confocal light microscopy to provide information about the structural changes occurring in polymerized fibrin during fibrinolysis. Many of the results of these experiments were unexpected and suggest some aspects of potential molecular mechanisms of fibrinolysis, which will also be described here.


2019 ◽  
Vol 116 (32) ◽  
pp. 16121-16126 ◽  
Author(s):  
Ying Zhang ◽  
Yan Xiong ◽  
Renyi Liu ◽  
Hong-Wei Xue ◽  
Zhenbiao Yang

Grain size is a key factor for determining grain yield in crops and is a target trait for both domestication and breeding, yet the mechanisms underlying the regulation of grain size are largely unclear. Here we show that the grain size and yield of rice (Oryza sativa) is positively regulated by ROP GTPase (Rho-like GTPase from plants), a versatile molecular switch modulating plant growth, development, and responses to the environment. Overexpression of rice OsRac1ROP not only increases cell numbers, resulting in a larger spikelet hull, but also accelerates grain filling rate, causing greater grain width and weight. As a result, OsRac1 overexpression improves grain yield in O. sativa by nearly 16%. In contrast, down-regulation or deletion of OsRac1 causes the opposite effects. RNA-seq and cell cycle analyses suggest that OsRac1 promotes cell division. Interestingly, OsRac1 interacts with and regulates the phosphorylation level of OsMAPK6, which is known to regulate cell division and grain size in rice. Thus, our findings suggest OsRac1 modulates rice grain size and yield by influencing cell division. This study provides insights into the molecular mechanisms underlying the control of rice grain size and suggests that OsRac1 could serve as a potential target gene for breeding high-yield crops.


2006 ◽  
Vol 84 (1) ◽  
pp. 49-59 ◽  
Author(s):  
Aaron Y. Lai ◽  
Kathryn G. Todd

The precise role of microglia in stroke and cerebral ischemia has been the subject of debate for a number of years. Microglia are capable of synthesizing numerous soluble and membrane-bound biomolecules, some known to be neuroprotective, some neurotoxic, whereas others have less definitive bioactivities. The molecular mechanisms through which microglia activate these molecules have thus become an important area of ischemia research. Here we provide a survey review that summarizes the key actions of microglial factors in cerebral ischemia including complement proteins, chemokines, pro-inflammatory cytokines, neurotrophic factors, hormones, and proteinases, as well several important messenger molecules that play a part in how these factors respond to extracellular signals during ischemic injuries. We also provide some new perspectives on how microglial intracellular signaling may contribute to the seemingly contradictory roles of several microglial effector molecules.


Foods ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1907
Author(s):  
Shambhavi Yadav ◽  
Joana Carvalho ◽  
Isabel Trujillo ◽  
Marta Prado

The olive fruit, a symbol of Mediterranean diets, is a rich source of antioxidants and oleic acid (55–83%). Olive genetic resources, including cultivated olives (cultivars), wild olives as well as related subspecies, are distributed widely across the Mediterranean region and other countries. Certain cultivars have a high commercial demand and economical value due to the differentiating organoleptic characteristics. This might result in economically motivated fraudulent practices and adulteration. Hence, tools to ensure the authenticity of constituent olive cultivars are crucial, and this can be achieved accurately through DNA-based methods. The present review outlines the applications of microsatellite markers, one of the most extensively used types of molecular markers in olive species, particularly referring to the use of these DNA-based markers in cataloging the vast olive germplasm, leading to identification and authentication of the cultivars. Emphasis has been given on the need to adopt a uniform platform where global molecular information pertaining to the details of available markers, cultivar-specific genotyping profiles (their synonyms or homonyms) and the comparative profiles of oil and reference leaf samples is accessible to researchers. The challenges of working with microsatellite markers and efforts underway, mainly advancements in genotyping methods which can be effectively incorporated in olive oil varietal testing, are also provided. Such efforts will pave the way for the development of more robust microsatellite marker-based olive agri-food authentication platforms.


2018 ◽  
Author(s):  
Evgeny Zatulovskiy ◽  
Daniel F. Berenson ◽  
Benjamin R. Topacio ◽  
Jan M. Skotheim

Cell size is fundamental to function in different cell types across the human body because it sets the scale of organelle structures, biosynthesis, and surface transport1,2. Tiny erythrocytes squeeze through capillaries to transport oxygen, while the million-fold larger oocyte divides without growth to form the ~100 cell pre-implantation embryo. Despite the vast size range across cell types, cells of a given type are typically uniform in size likely because cells are able to accurately couple cell growth to division3–6. While some genes whose disruption in mammalian cells affects cell size have been identified, the molecular mechanisms through which cell growth drives cell division have remained elusive7–12. Here, we show that cell growth acts to dilute the cell cycle inhibitor Rb to drive cell cycle progression from G1 to S phase in human cells. In contrast, other G1/S regulators remained at nearly constant concentration. Rb is a stable protein that is synthesized during S and G2 phases in an amount that is independent of cell size. Equal partitioning to daughter cells of chromatin bound Rb then ensures that all cells at birth inherit a similar amount of Rb protein. RB overexpression increased cell size in tissue culture and a mouse cancer model, while RB deletion decreased cell size and removed the inverse correlation between cell size at birth and the duration of G1 phase. Thus, Rb-dilution by cell growth in G1 provides a long-sought cell autonomous molecular mechanism for cell size homeostasis.


2018 ◽  
Author(s):  
Kimberley N. Babos ◽  
Kate E. Galloway ◽  
Kassandra Kisler ◽  
Madison Zitting ◽  
Yichen Li ◽  
...  

AbstractAlthough cellular reprogramming continues to generate new cell types, reprogramming remains a rare cellular event. The molecular mechanisms that limit reprogramming, particularly to somatic lineages, remain unclear. By examining fibroblast-to-motor neuron conversion, we identify a previously unappreciated dynamic between transcription and replication that determines reprogramming competency. Transcription factor overexpression forces most cells into states that are refractory to reprogramming and are characterized by either hypertranscription with little cell division, or hyperproliferation with low transcription. We identify genetic and chemical factors that dramatically increase the number of cells capable of both hypertranscription and hyperproliferation. Hypertranscribing, hyperproliferating cells reprogram at 100-fold higher, near-deterministic rates. We demonstrate that elevated topoisomerase expression endows cells with privileged reprogramming capacity, suggesting that biophysical constraints limit cellular reprogramming to rare events.


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