The Eukaryotic Cell Originated in the Integration and Redistribution of Hyperstructures from Communities of Prokaryotic Cells Based on Molecular Complementarity

Norris, Victor; Root‐Bernstein, Robert

doi:10.3390/ijms10062611

Cited by 12 publications

(11 citation statements)

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“…The biofilm is structured, possessing chemical gradients (aerobic to anaerobic for example [100]) and channels for the movement of nutrients [85][86][87]. Roles for biofilm matrices in eukaryogenesis have been proposed previously [101,102], although the mechanisms invoked differ from those discussed here. Jeckely [101] proposed that early eukaryotic evolution occurred in a social biofilm-like context, with a sub-set of cells in the community behaving as social cheaters.…”

Section: Extracellular Matrices As Models For the Third-spacementioning

confidence: 81%

“…Phagocytosis allows the subsequent uptake and incorporation of mitochondrial precursors as endosymbionts. Norris and Root-Bernstein [102] suggest that eukaryotes evolved from a mutualistic prokaryotic social structure such as a mat, biofilm or colony that underwent the exchange of "hyperstructures" (essentially pre-existing functional modules) between multiple cell types. This was achieved by the physical merger of the partner cells into a "meta-cell" that then underwent a process of integration and compaction or streamlining of structures to generate an entity more closely resembling a eukaryote.…”

Section: Extracellular Matrices As Models For the Third-spacementioning

confidence: 99%

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Division of labour in a matrix, rather than phagocytosis or endosymbiosis, as a route for the origin of eukaryotic cells

Bateman

2020

Biol Direct

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Two apparently irreconcilable models dominate research into the origin of eukaryotes. In one model, amitochondrial proto-eukaryotes emerged autogenously from the last universal common ancestor of all cells. Proto-eukaryotes subsequently acquired mitochondrial progenitors by the phagocytic capture of bacteria. In the second model, two prokaryotes, probably an archaeon and a bacterial cell, engaged in prokaryotic endosymbiosis, with the species resident within the host becoming the mitochondrial progenitor. Both models have limitations. A search was therefore undertaken for alternative routes towards the origin of eukaryotic cells. The question was addressed by considering classes of potential pathways from prokaryotic to eukaryotic cells based on considerations of cellular topology. Among the solutions identified, one, called here the "third-space model", has not been widely explored. A version is presented in which an extracellular space (the third-space), serves as a proxy cytoplasm for mixed populations of archaea and bacteria to "merge" as a transitionary complex without obligatory endosymbiosis or phagocytosis and to form a precursor cell. Incipient nuclei and mitochondria diverge by division of labour. The third-space model can accommodate the reorganization of prokaryote-like genomes to a more eukaryote-like genome structure. Nuclei with multiple chromosomes and mitosis emerge as a natural feature of the model. The model is compatible with the loss of archaeal lipid biochemistry while retaining archaeal genes and provides a route for the development of membranous organelles such as the Golgi apparatus and endoplasmic reticulum. Advantages, limitations and variations of the "third-space" models are discussed. Reviewers: This article was reviewed by Damien Devos, Buzz Baum and Michael Gray.

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Section: Extracellular Matrices As Models For the Third-spacementioning

confidence: 81%

Section: Extracellular Matrices As Models For the Third-spacementioning

confidence: 99%

Division of labour in a matrix, rather than phagocytosis or endosymbiosis, as a route for the origin of eukaryotic cells

Bateman

2020

Biol Direct

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“…What is effectively a paradigm-shift has taken the form of a paradigm slide. The new paradigm is beginning to have an effect on origins of life studies [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

DNA Movies and Panspermia

Norris

Grondin

2011

Life

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There are several ways that our species might try to send a message to another species separated from us by space and/or time. Synthetic biology might be used to write an epitaph to our species, or simply “Kilroy was here”, in the genome of a bacterium via the patterns of either (1) the codons to exploit Life's non-equilibrium character or (2) the bases themselves to exploit Life's quasi-equilibrium character. We suggest here how DNA movies might be designed using such patterns. We also suggest that a search for mechanisms to create and preserve such patterns might lead to a better understanding of modern cells. Finally, we argue that the cutting-edge microbiology and synthetic biology needed for the Kilroy project would put origin-of-life studies in the vanguard of research.

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“…Molecules aggregate into highly ordered, functional units at varying levels of complexity ranging from macromolecular complexes and organelles to cells, from cells to tissues and organs, and finally to the organism itself. The organizing principle at every level of organization is molecular complementarity -the intrinsic property of some molecules to take on structures and bonding patterns that permit them to interact reversibly with a select group of other molecules, macromolecules, or supra-molecular aggregates or cells (Root- Bernstein and Dillon, 1997;Hunding, et al, 2006;Norris and Root-Bernstein, 2009). Living organisms are, in short, comprised of highly-integrated, molecularly-complementary networks (Root-Bernstein, 2012;Csermely, 2006).…”

Section: Background: What Function Did the Immune System Evolve To Sementioning

confidence: 99%

<strong>A General Theory of Autoimmune Disease Causation: Integrating Innate and Adaptive Immunity, Altered Antigen Processing, Sex and Genetic Predispositions, and Microbiome Effects</strong>

Root‐Bernstein¹

2019

Preprint

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Current theories of autoimmunity are diverse, sometimes contradictory, and suffer from incompleteness. Although substantial evidence exists that adaptive and innate immunity, sex, genetic predisposition, and the microbiome all play essential roles in autoimmune disease etiologies and pathogenesis, and that antigen processing is altered during disease induction, no existing theory integrates all of these factors through a single, coherent mechanism. In an attempt to focus the field on the need to elucidate such an integrative mechanism, I propose one possibility here that, if nothing else, helps to identify the nature of the problems that need to be addressed. My theory is that autoimmune diseases are induced by normal immunological responses to unique pairs of complementary antigens, at least one of which is a molecular mimic of a host target.  Each antigen in the complementary pair induces a complementary immune response (T or B cell); although each immune response is idiotypic in origin, the antigenic complementarity results in what appears to be an idiotype-anti-idiotype relationship between the responses. Additionally, because of the antigenic complementarity, each immune response mimics one of antigens, abrogating the distinction between self and non-self. If at least one of the antigens mimics a host antigen, then the resulting immunological civil war spreads to a host tissue. Complementary antigens also alter antigen processing so that antigens that would normally be proteolytically digested are presented by the major histocompatibility complex (MHC) to T and B cell receptors inducing a cross-reactive immune response. The resulting civil war is supported by the innate immune system due to the complementarity of the initiating antigens.. Complementary antigens stimulate synergistic toll-like receptors (TLR) and/or nucleotide-binding oligomerization receptors (NOD) resulting in up-regulation of cytokine production and further stimulation of the adaptive immune response. Because the immune responses (e.g., antibodies) mimic the initiating antigens, this synergistic activation of innate immunity becomes chronic. Additionally, TLR and NOD function are highly sensitive to sex hormones, some becoming up-regulated and some down-regulated in the presence of either testosterone or estrogens. This sensitivity explains how sex modifies susceptibility to autoimmune diseases. Genetic mutations in TLR, NOD and MHC further alter antigen presentation and the degree to which antigens stimulate an immune response explaining how genetics also modifies susceptibility. Finally, sex hormones also alter the host microbiome, which in turn modulates autoimmune disease risk by shaping the immunological nature of self and by mediating susceptibility to microbial infection.  Moreover, it appears that the microbiome camouflages itself from the immune system by mimicking the host antigenic repertoire; the mimicry between the antigens of the microbiome and the host results in selective attacks on microbiome constituents concomitant with any autoimmune attack on host tissues. This antigenic complementarity theory thereby integrates all major elements known to affect, or be affected by, autoimmune diseases and provides a set of testable implications.

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The Eukaryotic Cell Originated in the Integration and Redistribution of Hyperstructures from Communities of Prokaryotic Cells Based on Molecular Complementarity

Cited by 12 publications

References 95 publications

Division of labour in a matrix, rather than phagocytosis or endosymbiosis, as a route for the origin of eukaryotic cells

Division of labour in a matrix, rather than phagocytosis or endosymbiosis, as a route for the origin of eukaryotic cells

DNA Movies and Panspermia

<strong>A General Theory of Autoimmune Disease Causation: Integrating Innate and Adaptive Immunity, Altered Antigen Processing, Sex and Genetic Predispositions, and Microbiome Effects</strong>

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