scholarly journals Emergence of multicellularity in a model of cell growth, death and aggregation under size-dependent selection

2015 ◽  
Vol 12 (102) ◽  
pp. 20140982 ◽  
Author(s):  
Salva Duran-Nebreda ◽  
Ricard Solé

How multicellular life forms evolved from unicellular ones constitutes a major problem in our understanding of the evolution of our biosphere. A recent set of experiments involving yeast cell populations have shown that selection for faster sedimenting cells leads to the appearance of stable aggregates of cells that are able to split into smaller clusters. It was suggested that the observed evolutionary patterns could be the result of evolved programmes affecting cell death. Here, we show, using a simple model of cell–cell interactions and evolving adhesion rates, that the observed patterns in cluster size and localized mortality can be easily interpreted in terms of waste accumulation and toxicity-driven apoptosis. This simple mechanism would have played a key role in the early evolution of multicellular life forms based on both aggregative and clonal development. The potential extensions of this work and its implications for natural and synthetic multicellularity are discussed.

Author(s):  
M. A. Listvan ◽  
R. P. Andres

Knowledge of the function and structure of small metal clusters is one goal of research in catalysis. One important experimental parameter is cluster size. Ideally, one would like to produce metal clusters of regulated size in order to characterize size-dependent cluster properties.A source has been developed which is capable of producing microscopic metal clusters of controllable size (in the range 5-500 atoms) This source, the Multiple Expansion Cluster Source, with a Free Jet Deceleration Filter (MECS/FJDF) operates as follows. The bulk metal is heated in an oven to give controlled concentrations of monomer and dimer which were expanded sonically. These metal species were quenched and condensed in He and filtered to produce areosol particles of a controlled size as verified by mass spectrometer measurements. The clusters were caught on pre-mounted, clean carbon films. The grids were then transferred in air for microscopic examination. MECS/FJDF was used to produce two different sizes of silver clusters for this study: nominally Ag6 and Ag50.


Author(s):  
Sandra M. Lang ◽  
Thorsten M. Bernhardt ◽  
Joost M. Bakker ◽  
Robert N. Barnett ◽  
Uzi Landman

2020 ◽  
Vol 10 ◽  
Author(s):  
Michelle Hu ◽  
Kermit L. Carraway

A major confounding issue in the successful treatment of cancer is the existence of tumor cell populations that resist therapeutic agents and regimens. While tremendous effort has gone into understanding the biochemical mechanisms underlying resistance to each traditional and targeted therapeutic, a broader approach to the problem may emerge from the recognition that existing anti-cancer agents elicit their cytotoxic effects almost exclusively through apoptosis. Considering the myriad mechanisms cancer cells employ to subvert apoptotic death, an attractive alternative approach would leverage programmed necrotic mechanisms to side-step therapeutic resistance to apoptosis-inducing agents. Lysosomal cell death (LCD) is a programmed necrotic cell death mechanism that is engaged upon the compromise of the limiting membrane of the lysosome, a process called lysosomal membrane permeabilization (LMP). The release of lysosomal components into the cytosol upon LMP triggers biochemical cascades that lead to plasma membrane rupture and necrotic cell death. Interestingly, the process of cellular transformation appears to render the limiting lysosomal membranes of tumor cells more fragile than non-transformed cells, offering a potential therapeutic window for drug development. Here we outline the concepts of LMP and LCD, and discuss strategies for the development of agents to engage these processes. Importantly, the potential exists for existing cationic amphiphilic drugs such as antidepressants, antibiotics, antiarrhythmics, and diuretics to be repurposed to engage LCD within therapy-resistant tumor cell populations.


2021 ◽  
Vol 95 (S1) ◽  
pp. S120-S127
Author(s):  
Dengxue Ma ◽  
Yaoyao Wei ◽  
Guokui Liu ◽  
Qiying Xia

2018 ◽  
Vol 315 (5) ◽  
pp. R879-R894 ◽  
Author(s):  
Jon F. Harrison

Hypometric scaling of aerobic metabolism [larger organisms have lower mass-specific metabolic rates (MR/g)] is nearly universal for interspecific comparisons among animals, yet we lack an agreed upon explanation for this pattern. If physiological constraints on the function of larger animals occur and limit MR/g, these should be observable as direct constraints on animals of extant species and/or as evolved responses to compensate for the proposed constraint. There is evidence for direct constraints and compensatory responses to O2 supply constraint in skin-breathing animals, but not in vertebrates with gas-exchange organs. The duration of food retention in the gut is longer for larger birds and mammals, consistent with a direct constraint on nutrient uptake across the gut wall, but there is little evidence for evolving compensatory responses to gut transport constraints in larger animals. Larger placental mammals (but not marsupials or birds) show evidence of greater challenges with heat dissipation, but there is little evidence for compensatory adaptations to enhance heat loss in larger endotherms, suggesting that metabolic rate (MR) more generally balances heat loss for thermoregulation in endotherms. Size-dependent patterns in many molecular, physiological, and morphological properties are consistent with size-dependent natural selection, such as stronger selection for neurolocomotor performance and growth rate in smaller animals and stronger selection for safety and longevity in larger animals. Hypometric scaling of MR very likely arises from different mechanisms in different taxa and conditions, consistent with the diversity of scaling slopes for MR.


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