FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2479766063> ?p ?o ?g. }

• W2479766063 endingPage "R607" @default.
• W2479766063 startingPage "R594" @default.
• W2479766063 abstract "Unicellular, planktonic, prokaryotic and eukaryotic photoautotrophs (phytoplankton) have an ancient evolutionary history on Earth during which time they have played key roles in the regulation of marine food webs, biogeochemical cycles, and Earth’s climate. Since they represent the basis of aquatic ecosystems, the manner in which phytoplankton die critically determines the flow and fate of photosynthetically fixed organic matter (and associated elements), ultimately constraining nutrient flow. Programmed cell death (PCD) and associated pathway genes, which are triggered by a variety of abiotic (nutrient, light, osmotic) and biotic (virus infection, allelopathy) environmental stresses, have an integral grip on cell fate, and have shaped the ecological success and evolutionary trajectory of diverse phytoplankton lineages. A combination of physiological, biochemical, and genetic techniques in model algal systems has demonstrated a conserved molecular and mechanistic framework of stress surveillance, signaling, and death activation pathways, involving collective and coordinated participation of organelles, redox enzymes, metabolites, and caspase-like proteases. This mechanistic understanding has provided insight into the integration of sensing and transduction of stress signals into cellular responses, and the mechanistic interfaces between PCD, cell stress and virus infection pathways. It has also provided insight into the evolution of PCD in unicellular photoautotrophs, the impact of PCD on the fate of natural phytoplankton assemblages and its role in aquatic biogeochemical cycles. Unicellular, planktonic, prokaryotic and eukaryotic photoautotrophs (phytoplankton) have an ancient evolutionary history on Earth during which time they have played key roles in the regulation of marine food webs, biogeochemical cycles, and Earth’s climate. Since they represent the basis of aquatic ecosystems, the manner in which phytoplankton die critically determines the flow and fate of photosynthetically fixed organic matter (and associated elements), ultimately constraining nutrient flow. Programmed cell death (PCD) and associated pathway genes, which are triggered by a variety of abiotic (nutrient, light, osmotic) and biotic (virus infection, allelopathy) environmental stresses, have an integral grip on cell fate, and have shaped the ecological success and evolutionary trajectory of diverse phytoplankton lineages. A combination of physiological, biochemical, and genetic techniques in model algal systems has demonstrated a conserved molecular and mechanistic framework of stress surveillance, signaling, and death activation pathways, involving collective and coordinated participation of organelles, redox enzymes, metabolites, and caspase-like proteases. This mechanistic understanding has provided insight into the integration of sensing and transduction of stress signals into cellular responses, and the mechanistic interfaces between PCD, cell stress and virus infection pathways. It has also provided insight into the evolution of PCD in unicellular photoautotrophs, the impact of PCD on the fate of natural phytoplankton assemblages and its role in aquatic biogeochemical cycles. Biogeochemical cycles in aquatic ecosystems are driven entirely by microorganisms. Phytoplankton — a diverse group of photosynthetic microorganisms that drift with the currents and encompass ancient cyanobacterial and derived, independently evolving ‘red’ and ‘green’ plastid eukaryotic lineages [1Falkowski P.G. Katz M.E. Knoll A.H. Quigg A. Raven J.A. Schofield O. Taylor F.J.R. The evolution of modern eukaryotic phytoplankton.Science. 2004; 305: 354-360Crossref PubMed Scopus (694) Google Scholar] — play a prominent role. They are responsible for nearly half the global carbon-based primary production, are the basis of aquatic foodwebs, and directly influence their environment and the organisms within it [2Falkowski P.G. Barber R.T. Smetacek V. Biogeochemical controls and feedbacks on ocean primary production.Science. 1998; 281: 200-206Crossref PubMed Scopus (1188) Google Scholar, 3Redfield A.C. The biological control of chemical factors in the environment.Am. Sci. 1958; 46: 205-221Google Scholar]. Perhaps the most striking example of their collective influence is the oxygenation of Earth’s atmosphere ca. 2.2 billion years ago (Ga) [4Bekker A. Holland H.D. Wang P.-L. Rumble III, D. Stein H.J. Hannah J.L. Coetzee L.L. Beukes N.J. Dating the rise of atmospheric oxygen.Nature. 2004; 427: 117-120Crossref PubMed Scopus (0) Google Scholar], a development that set the stage for the evolution of higher animals (∼0.7 Ga) [5Knoll A.H. Life on a Young Planet: The First Three Billion Years of Evolution on Earth. Princeton University Press, Princeton, NJ2003Google Scholar]. In order to maintain biogeochemical cycles throughout billions of years of Earth’s history, phytoplankton must not only grow, but also die. Phytoplankton account for <1% of Earth’s biomass but are responsible for nearly 50% of global annual carbon-based primary productivity [6Field C.B. Behrenfeld M.J. Randerson J.T. Falkowski P. Primary production of the biosphere: integrating terrestrial and oceanic components.Science. 1998; 281: 237-240Crossref PubMed Scopus (2120) Google Scholar]. Steady-state maintenance of this high production/biomass ratio implies that, on average, these organisms grow, die and are replaced weekly [7Valiela I. Marine Ecological Processes. Springer-Verlag, New York1995Crossref Google Scholar]. Given this fact, it’s puzzling that a misconception largely drove our traditional understanding of phytoplankton ecophysiology. It had been assumed that these cells were immortal, growing indefinitely by binary fission unless eaten by heterotrophic zooplankton (animals that drift with currents) or removed by irreversible sinking into the deep ocean as aggregated particles, both thought to comprise independent ecosystem pathways (Figure 1). This view fundamentally changed towards the end of the 20th century, when it became clear that phytoplankton often die spontaneously upon encountering adverse abiotic or biotic environmental conditions. Indeed, substantial cell death by lysis has been documented in field populations, with some estimates exceeding 50% of phytoplankton growth [8vanBoekel W.H.M. Hansen F.C. Riegman R. Bak R.P.M. Lysis-induced decline of a Phaeocystis spring bloom and coupling with the microbial foodweb.Mar. Ecol. Prog. Ser. 1992; 81: 269-276Crossref Google Scholar, 9Agustí S. Satta M.P. Mura M.P. Benavent E. Dissolved esterase activity as a trace of phytoplankton lysis: Evidence of high phytoplankton lysis rates in the northwestern Mediterranean.Limnol. Oceanogr. 1998; 43: 1836-1849Crossref Google Scholar, 10Brussaard C.P.D. Riegman R. Noordeloos A.A.M. Cadée G.C. Witte H. Kop A.J. Nieuwland G. Duyl F.C.v. Bak R.P.M. Effects of grazing, sedimentation and phytoplankton cell lysis on the structure of a coastal pelagic food web.Mar. Ecol. Prog. Ser. 1995; 123: 259-271Crossref Google Scholar]. Hence, important loss processes independent of grazing by heterotrophs must exist and might explain how an average of ∼50% of global primary production is consumed by bacteria [11Cole J.J. Findlay S. Pace M.L. Bacterioplankton production in fresh and saltwater ecosystems: a cross-system overview.Mar. Ecol. Prog. Ser. 1988; 43: 1-10Crossref Google Scholar]. The primary mechanism invoked by microbial ecologists to explain these high lysis rates of phytoplankton populations has been predatory infection by lytic viruses, which infect a host cell, propagate and, subsequently, release viral progeny from a lysed microbial cell together with dissolved organic matter into the surrounding water. Viruses are now known to be ubiquitous and critical components of marine ecosystems, reaching abundances of 107–108 viruses per milliliter of surface seawater, which exceeds bacterial and phytoplankton abundance by at least an order of magnitude. Viruses that are pathogenic to a variety of phytoplankton species can routinely be isolated from seawater with detailed knowledge of the dynamics and physiology of viral infection coming primarily from cultured virus–host systems. The development of novel diagnostic biomolecular techniques to detect infection by specific microalgal viruses and assess the accompanying physiological changes have not only convincingly demonstrated evidence of virus impact on bloom demise but also revealed co-evolutionary, functional links between virus infection and autocatalytic, programmed cell death (PCD) pathways within widespread, globally distributed, ecologically important phytoplankton species [12Bidle K.D. The molecular ecophysiology of programmed cell death in marine phytoplankton.Annu. Rev. Mar. Sci. 2015; 7: 24.21-24.35Crossref Scopus (0) Google Scholar, 13Bidle K.D. Vardi A. A chemical arms race at sea mediates algal host–virus interactions.Curr. Opin. Microbiol. 2011; 14: 449-457Crossref PubMed Scopus (0) Google Scholar, 14Fulton J.M. Fredricks H.F. Bidle K.D. Vardi A. Kendrick J. DiTullio G.R. Mooy B.A.S.V. Novel molecular determinants of viral susceptibility and resistance in the lipidome of Emiliania huxleyi.Environ. Microbiol. 2014; 16: 1137-1149Crossref PubMed Scopus (31) Google Scholar, 15Rohwer F. Thurber R.V. Viruses manipulate the marine environment.Nature. 2009; 459: 207-212Crossref PubMed Scopus (0) Google Scholar, 16Vardi A. Haramaty L. VanMooy B.A.S. Fredricks H.F. Kimmance S.A. Larsen A. Bidle K.D. Host–virus dynamics and subcellular controls of cell fate in a natural coccolithophore population.Proc. Natl. Acad. Sci. USA. 2012; 109: 19327-19332Crossref PubMed Scopus (0) Google Scholar, 17Vardi A. Mooy B.A.S.V. Fredricks H.F. Popendorf K.J. Ossolinski J.E. Haramaty L. Bidle K.D. Viral glycosphingolipids induce lytic infection and cell death in marine phytoplankton.Science. 2009; 326: 861-865Crossref PubMed Scopus (102) Google Scholar]. The induction of autocatalytic PCD by environmental stresses (e.g., cell age, nutrient deprivation, high light, excessive salt, or oxidative stress; detailed below) in both prokaryotic and eukaryotic phytoplankton provides another mechanism to explain high lysis rates, independent of viral attack. It is now abundantly clear that diverse phytoplankton lineages activate conserved autocatalytic PCD pathways upon encountering adverse abiotic or biotic environmental conditions and that this intrinsic, cellular mechanism of death shares core components of death pathways in higher plants and animals, fundamentally influences the flow of photosynthetically fixed organic matter (and associated elements) through the main ecosystem foodweb pathways — grazer food web, vertical sinking flux and microbial loop — and serves to lubricate ocean biogeochemistry (Figure 1) [12Bidle K.D. The molecular ecophysiology of programmed cell death in marine phytoplankton.Annu. Rev. Mar. Sci. 2015; 7: 24.21-24.35Crossref Scopus (0) Google Scholar, 18Bidle K.D. Falkowski P.G. Cell death in planktonic photosynthetic microorganisms.Nat. Rev. Microbiol. 2004; 2: 643-655Crossref PubMed Scopus (0) Google Scholar, 19Kirchman D.L. Phytoplankton death in the sea.Nature. 1999; 398: 293-294Crossref Scopus (0) Google Scholar]. Here, I discuss the current state of knowledge of PCD in unicellular photoautotrophs, including cellular mechanisms of activation and regulation, evolutionary establishment and ecological significance, interaction with virus infection, sensing and transduction into cellular responses, and its impact on aquatic biogeochemical cycles. The diagnosis of phytoplankton PCD has been critically informed by an extensive mechanistic knowledge of PCD pathways in diverse organisms, including single-celled bacteria, protists and fungi, as well as multicellular land plants and higher animals. These include apoptosis [20Lockshin R.A. Williams C.M. Programmed cell death-I. Cytolytic enzymes in relation to the breakdown of the intersegmental muscles of silkmoths.J. Insect. Physiol. 1965; 11: 831-844Crossref PubMed Google Scholar, 21Kerr J.F. Wyllie A.H. Currie A.R. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.Br. J. Cancer. 1972; 26: 239-257Crossref PubMed Google Scholar], paraptosis [22Sperandio S. Belle I.d. Bredesen D.E. An alternative, nonapoptotic form of programmed cell death.Proc. Natl. Acad. Sci. USA. 2000; 97: 14376-14381Crossref PubMed Scopus (616) Google Scholar], ferrapoptosis [23Dixon S.J. Lemberg K.M. Lamprecht M.R. Skouta R. Zaitsev E.M. Gleason C.E. Patel D.N. Bauer A.J. Cantley A.M. Yang W.S. et al.Ferroptosis: an iron-dependent form of nonapoptotic cell death.Cell. 2012; 149: 1060-1072Abstract Full Text Full Text PDF PubMed Scopus (525) Google Scholar] and autophagy [24Denton D. Nicolson S. Kumar S. Cell death by autophagy: facts and apparent artefacts.Cell Death Differ. 2011; 19: 87-95Crossref PubMed Scopus (0) Google Scholar, 25Shemi A. Ben-Dor S. Vardi A. Elucidating the composition and conservation of the autophagy pathway in photosynthetic eukaryotes.Autophagy. 2015; 11: 701-715Crossref PubMed Google Scholar], with each type being supported by cytological and biochemical evidence and occurring under disparate circumstances. As originally defined in animals [21Kerr J.F. Wyllie A.H. Currie A.R. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.Br. J. Cancer. 1972; 26: 239-257Crossref PubMed Google Scholar], apoptosis refers to specific morphological changes that occur during genetically controlled cell death, including cell shrinkage, chromatin condensation, DNA fragmentation, and blebbing of the cell membrane. These morphological traits are often used to distinguish apoptotic cell death from necrosis, which results from acute and irreversible cellular injury and leads to general swelling of the plasma membrane, the presence of chromatin clusters, and DNA strand breaks [26Golstein P. Kroemer G. Cell death by necrosis: towards a molecular definition.Trends Biochem. Sci. 2006; 32: 37-43Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, 27Laporte C. Kosta A. Klein G. Aubry L. Lam D. Tresse E. Luciani M.F. Goldstein P. A necrotic cell death model in a protist.Cell Death Differ. 2006; 14: 266-274Crossref PubMed Scopus (0) Google Scholar, 28Vanlangenakker N. Berghe T.V. Vandenabeele P. Many stimuli pull the necrotic trigger, an overview.Cell Death Differ. 2011; 19: 75-86Crossref PubMed Scopus (0) Google Scholar]. Definitions of PCD have broadened to include a variety of diverse, genetically controlled, active cellular self-destruction pathways, many of which have been observed in unicellular marine phytoplankton. These include: paraptosis, a nonapoptotic form of PCD characterized by chromatin spotting without DNA fragmentation, extensive cytoplasmic swelling and vacuolization, and alternative caspase activity; aponecrosis, a chimeric form of cell death that shares dynamic, molecular, and morphological features with both apoptosis and necrosis [29Jiménez C. Capasso J.M. Edelstein C.L. Rivard C.J. Lucia S. Breusegem S. Berl T. Segovia M. Different ways to die: cell death modes of the unicellular chlorophyte Dunaliella viridis exposed to various environmental stresses are mediated by the caspase-like activity DEVDase.J. Exp. Bot. 2009; 60: 815-828Crossref PubMed Scopus (56) Google Scholar]; and autophagy, a highly conserved cellular process (protists to animals) that involves atg genes and the formation of autophagosomes, which interact with lysosomes to engulf cellular constituents. Intriguingly, autophagy has been linked to both cell survival and death, depending on the stress. Ferroptosis, an iron-dependent cell death, is similar to glutamate-induced excitotoxicity but distinct from apoptosis, necrosis, and autophagy. PCD has long been regarded as a hallmark of multicellular, higher eukaryotes [30Skulachev V.P. The programmed cell death phenomena, aging, and the Samurai law of biology.Exp. Gerontol. 2001; 36: 995-1024Crossref PubMed Scopus (0) Google Scholar], since it is universally required for their development, function, and ultimate survival. Traditional distinctions between PCD and necrosis in metazoans have made assessment of cell death in unicellular organisms, like phytoplankton, more difficult to define based on these criteria. Nevertheless, PCD has been identified in broadly diverse unicellular heterotrophic organisms such as bacteria [31Bayles K.W. Bacterial programmed cell death: making sense of a paradox.Nat. Rev. Microbiol. 2014; 12: 63-69Crossref PubMed Scopus (62) Google Scholar, 32Rice K.C. Bayles K.W. Death’s toolbox: examining the molecular components of bacterial programmed cell death.Mol. Microbiol. 2003; 50: 729-738Crossref PubMed Scopus (0) Google Scholar, 33Yarmolinsky M.B. Programmed cell death in bacterial populations.Science. 1995; 267: 836-837Crossref PubMed Google Scholar], yeast [34Fröhlich K.-U. Madeo F. Apoptosis in yeast: A monocellular organism exhibits altruistic behaviour.FEBS Lett. 2000; 473: 6-9Crossref PubMed Scopus (0) Google Scholar], and protozoa [35Ameisen J.C. Idziorek T. Billaut-Mulot O. Loyens M. Tissier J.P. Potentier A. Ouaissi M.A. Apoptosis in a unicellular eukaryote (Trypazoma cruzi): implications for the evolutionary origin and role of programmed cell death in the control of cell proliferation, differentiation and survival.Cell Death Differ. 1995; 2: 285-300PubMed Google Scholar, 36Arnoult D. Akarid K. Grodet A. Petit P.X. Estaquier J. Ameisen J.C. On the evolution of programmed cell death: apoptosis of the unicellular eukaryote Leishmania major involves cysteine proteinase activation and mitochondrion permeabilization.Cell Death Differ. 2002; 9: 65-81Crossref PubMed Scopus (0) Google Scholar], demonstrating that it is a fundamental feature of prokaryotic and eukaryotic, unicellular microbial life with ancient origins [37Ameisen J.C. On the origin, evolution, and nature of programmed cell death: a timeline of four billion years.Cell Death Differ. 2002; 9: 367-393Crossref PubMed Scopus (349) Google Scholar, 38Koonin E.V. Aravind L. Origin and evolution of eukaryotic apoptosis: the bacterial connection.Cell Death Differ. 2002; 9: 394-404Crossref PubMed Scopus (246) Google Scholar]. Genomic, physiological, morphological, and biochemical evidence of PCD — autocatalytic cell suicide in which an endogenous biochemical pathway leads to apoptotic-like morphological changes and, ultimately, cellular dissolution — has now been documented in phytoplankton lineages of cyanobacteria, which were present in marine ecosystems at least 2.8 billion years ago (Ga) [39Summons R.E. Jahnke L.L. Hope J.M. Logan G.A. 2-Methylhopanoids as biomarkers for cyanobacterial oxygenic photosynthesis.Nature. 1999; 400: 555-557Crossref Scopus (0) Google Scholar] and in diverse eukaryotic representatives of independently evolving ancient superfamilies (clusters of phyla), the ‘green’ and ‘red’ lineages, which inhabited coastal waterways by 1.4–1.9 Ga [1Falkowski P.G. Katz M.E. Knoll A.H. Quigg A. Raven J.A. Schofield O. Taylor F.J.R. The evolution of modern eukaryotic phytoplankton.Science. 2004; 305: 354-360Crossref PubMed Scopus (694) Google Scholar, 40Yoon H.S. Hackett J.D. Ciniglia C. Pinto G. Bhattacharya D. A molecular timeline for the origin of photosynthetic eukaryotes.Mol. Biol. Evol. 2004; 21: 809-818Crossref PubMed Scopus (508) Google Scholar] and were genetically transferred to multicellular plants in the latter half of Earth’s history (Figure 2). It remains one of the more enigmatic and intriguing aspects of microbial and cellular evolution and, as such, a variety of ecological and evolutionary drivers have been proposed for the maintenance of PCD-related genes in aquatic photosynthetic microbes over their ∼3 Ga evolutionary history (discussed below) [12Bidle K.D. The molecular ecophysiology of programmed cell death in marine phytoplankton.Annu. Rev. Mar. Sci. 2015; 7: 24.21-24.35Crossref Scopus (0) Google Scholar, 18Bidle K.D. Falkowski P.G. Cell death in planktonic photosynthetic microorganisms.Nat. Rev. Microbiol. 2004; 2: 643-655Crossref PubMed Scopus (0) Google Scholar, 25Shemi A. Ben-Dor S. Vardi A. Elucidating the composition and conservation of the autophagy pathway in photosynthetic eukaryotes.Autophagy. 2015; 11: 701-715Crossref PubMed Google Scholar, 41Franklin D.J. Brussaard C.P.D. Berges J.A. What is the role and nature of programmed cell death in phytoplankton ecology?.Eur. J. Phycol. 2006; 41: 1-14Crossref Scopus (91) Google Scholar, 42Nedelcu A.M. Driscoll W.W. Durand P.M. Herron M.D. Rashidi A. On the paradigm of altruistic suicide in the unicellular world.Evolution. 2011; 65: 3-20Crossref PubMed Scopus (64) Google Scholar]. Considerable attention has been paid over the past decade to experimentally elucidate the mechanistic controls of, genetic linkages to, and biochemical activities associated with algal PCD pathways. These efforts have answered fundamental questions about the nature of its activation and informed our collective thinking on the retention of an ostensibly counterintuitive pathway in unicellular algae — given the cell is the organism, death cannot inherently benefit the individual and is a first order control on organism fate. PCD pathway genes have a tight grip on the cell fate of diverse photoautotrophs in aquatic environments and are collectively hard-wired into genomes with an ancient evolutionary history spanning ∼3 Ga. This multifaceted genetic program must have some selective advantage to unicells or it would have been purged from genomes long ago. Various ecological and evolutionary drivers have been proposed. An intriguing and straightforward idea is that death represents a default pathway in biology. Cells indeed appear to be intrinsically programmed to self-destruct with cell survival depending on its effective and continued repression [37Ameisen J.C. On the origin, evolution, and nature of programmed cell death: a timeline of four billion years.Cell Death Differ. 2002; 9: 367-393Crossref PubMed Scopus (349) Google Scholar, 43Raff M.C. Social controls on cell survival and cell death.Nature. 1992; 356: 397-400Crossref PubMed Scopus (2353) Google Scholar, 44Ameisen J.C. The evolutionary origin and role of programmed cell death in single-celled organisms: a new view at executioners, mitochondria, host-pathogen interactions and the role of death in the process of natural selection.in: Lockshin R.A. Zakeri Z. Tilly J.L. When Cells Die: a Comprehensive Evaluation of Apoptosis and Programmed Cell Death. Wiley-Liss, New York1998: 3-56Google Scholar]. PCD pathways in diverse cell systems, including phytoplankton [45Moharikar S. D’Souza J.S. Rao B.J. A homologue of the defender against the apoptotic death gene (dad1) in UV-exposed Chlamydomonas cells is downregulated with the onset of programmed cell death.J. Biosci. 2007; 32: 261-270Crossref PubMed Scopus (0) Google Scholar], are littered with structurally related ‘inhibitors of apoptosis’ (IAP) proteins [46Deveraux Q.L. Reed J.C. IAP family proteins—suppressors of apoptosis.Genes Dev. 1999; 13: 239-252Crossref PubMed Google Scholar, 47Deveraux Q.L. Takahashi R. Salvesen G.S. Reed J.C. X-linked IAP is a direct inhibitor of cell-death proteases.Nature. 1997; 388: 300-304Crossref PubMed Scopus (1537) Google Scholar, 48Wilkinson J.C. Richter B.W.M. Wilkinson A.S. Burstein E. Rumble J.M. Balliu B. Duckett C.S. VIAF, a conserved inhibotr of apoptosis (IAP)-interacting factor that modulates caspase activation.J. Biol. Chem. 2004; 279: 51091-51099Crossref PubMed Scopus (0) Google Scholar], some tightly binding to caspases, efficiently inhibiting their activation and preventing apoptosis. It follows that a deficiency in death repression will automatically remove less fit cells from the population. As such, PCD in unicellular organisms might convey enhanced genetic and population fitness and represent an adaptation designed to benefit a population [33Yarmolinsky M.B. Programmed cell death in bacterial populations.Science. 1995; 267: 836-837Crossref PubMed Google Scholar, 34Fröhlich K.-U. Madeo F. Apoptosis in yeast: A monocellular organism exhibits altruistic behaviour.FEBS Lett. 2000; 473: 6-9Crossref PubMed Scopus (0) Google Scholar], whereby damaged cells are eliminated from a population and provide surviving cells with limiting nutrients. Indeed, the manner in which a phytoplankton cell dies directly impacts the fitness of its neighbouring cells [49Durand P.M. Rashidi A. Michod R.E. How an organism dies affects the fitness of its neighbors.Am. Nat. 2011; 177: 224-232Crossref PubMed Scopus (25) Google Scholar], the degree to which is influenced by phylogenetic relatedness [50Durand P.M. Choudhury R. Rashidi A. Michod R.E. Programmed death in a unicellular organism has species-specific fitness effects.Biol. Lett. 2014; 10: 20131088Crossref PubMed Scopus (9) Google Scholar]. Observations of community-wide PCD activation in natural populations of the coccolithophore Emiliania huxleyi [16Vardi A. Haramaty L. VanMooy B.A.S. Fredricks H.F. Kimmance S.A. Larsen A. Bidle K.D. Host–virus dynamics and subcellular controls of cell fate in a natural coccolithophore population.Proc. Natl. Acad. Sci. USA. 2012; 109: 19327-19332Crossref PubMed Scopus (0) Google Scholar] argue against purifying selection of PCD alleles within populations with documented genetic microdiversity [51Rynearson T.A. Armbrust E.V. Maintenance of clonal diversity during a spring bloom of the centric diatom Ditylum brightwellii.Mol. Ecol. Lett. 2005; 14: 1631-1640Crossref PubMed Scopus (0) Google Scholar] (Hinz et al., unpublished observations). Instead, these alleles may increase in frequency among closely related individuals if it favors the collective fitness of genes, as per the ‘kin selection’ model [52Hamilton W.D. The genetical evolution of social behavior.J. Theor. Biol. 1964; 7: 1-52Crossref PubMed Google Scholar]. Alternatively, PCD (and its associated molecular machinery) may play important roles in cell survival in different environmental niches. PCD-related genes may be an integral component of cellular differentiation and development pathways for specialized phytoplankton and ecophysiological strategies, such as those employed by nitrogen-fixing (diazotrophic) cyanobacteria [53Berman-Frank I. Lundgren P. Falkowski P. Nitrogen fixation and photosynthetic oxygen evolution in cyanobacteria.Res. Microbiol. 2003; 154: 157-164Crossref PubMed Scopus (0) Google Scholar] and sexual stages induced by abiotic and biotic challenges [54Frada M. Probert I. Allen M.J. Wilson W.H. Vargas C.D. The “Cheshire Cat” escape strategy of the coccolithophore Emiliania huxleyi in response to viral infection.Proc. Natl. Acad. Sci. USA. 2008; 105: 15944-15949Crossref PubMed Scopus (0) Google Scholar]. PCD-related genes have clearly been a mechanistic playground of co-evolutionary host–virus arms races with PCD-based virus exclusion strategies pre-empting viral replication [55Georgiou T. Yu Y.-T.N. Ekunwe S. Buttner M.J. Zuurmond A.-M. Kraal B. Kleanthous C. Snyder L. Specific peptide-activated proteolytic cleavage of Escherichia coli elongation factor Tu.Proc. Natl. Acad. Sci. USA. 1998; 95: 2891-2895Crossref PubMed Scopus (0) Google Scholar] or the viruses themselves requiring PCD induction for replication [56Bidle K.D. Haramaty L. Barcelos-Ramos J. Falkowski P.G. Viral activation and recruitment of metacaspases in the unicellular coccolithophorid, Emiliania huxleyi.Proc. Natl. Acad. Sci. USA. 2007; 104: 6049-6054Crossref PubMed Scopus (0) Google Scholar, 57Schatz D. Shemi A. Rosenwasser S. Sabanay H. Wolf S.G. Ben-Dor S. Vardi A. Hijacking of an autophagy-like process is essential for the life cycle of a DNA virus infecting oceanic algal blooms.New Phytol. 2014; 204: 854-863Crossref PubMed Scopus (0) Google Scholar]. PCD-related genes may have alternative physiological functions, participating in housekeeping, stress acclimation, or regulatory functions whereby retention and expression are of physiological benefit. Some death-related genes in unicellular phytoplankton appear to have dual roles, as determined by environmental conditions and cell history. In a broader context, the high and highly specific catalytic caspase-specific activity observed in diverse phyla of exponentially growing Archaea [58Bidle K.A. Haramaty L. Baggett N. Nannen J. Bidle K.D. Tantalizing evidence for archaeal caspase-like protein expression and activity and its role in cellular stress response.Environ. Microbiol. 2010; 12: 1161-1172Crossref PubMed Scopus (0) Google Scholar, 59Seth-Pasricha M. Bidle K.A. Bidle K.D. Specificity of archaeal caspase activity in the extreme halophile Haloferax volcanii.Environ. Microbiol. Rep. 2013; 5: 263-271Crossref PubMed Scopus (0) Google Scholar] implicates it as a core component of an ‘interactase’ of stress-related protein complexes involved in proper proteasome function and the unfolded protein response [60Seth-Pasricha M. Biochemical and physiological characterization of caspase activity in haloarchaea.in: Graduate Program in Microbiology and Molecular Genetics, Volume Ph.D. Rutgers University, New Brunswick, NJ2015: 138Google Scholar]. In light of the deep archaeal roots of eukaryotes [61Asplund-Samuelsson J. Bergman B. Larsson J. Prokaryotic caspase homologs: phylogenetic patterns and functional characteristics reveal considerable diversity.PLoS One. 2012; 7: e49888Crossref PubMed Scopus (0) Google Scholar, 62Hug L.A. Baker B.J. Anantharaman K. Brown C.T. Probst A.J. Castelle C.J. Butterfield C.N. Hernsdorf A.W. Amano Y. Ise K. et al.A new view of the tree of life.Nat. Microbiol. 2016; (16048)Crossref PubMed Scopus (192) Google Scholar, 63Spang A. Saw J.H. Jørgensen S.L. Zaremba-Niedzwiedzka K. Martijn J. Lind A.E. Eijk R.v. Schleper C. Guy L. Ett" @default.
• W2479766063 created "2016-08-23" @default.
• W2479766063 creator A5059955159 @default.
• W2479766063 date "2016-07-01" @default.
• W2479766063 modified "2023-10-18" @default.
• W2479766063 title "Programmed Cell Death in Unicellular Phytoplankton" @default.
• W2479766063 cites W1269597682 @default.
• W2479766063 cites W1529393898 @default.
• W2479766063 cites W1532877896 @default.
• W2479766063 cites W1542452066 @default.
• W2479766063 cites W1557686543 @default.
• W2479766063 cites W1560024199 @default.
• W2479766063 cites W1612113997 @default.
• W2479766063 cites W1619095826 @default.
• W2479766063 cites W1745634660 @default.
• W2479766063 cites W1797582458 @default.
• W2479766063 cites W1821918060 @default.
• W2479766063 cites W1831878317 @default.
• W2479766063 cites W1884746789 @default.
• W2479766063 cites W1939911045 @default.
• W2479766063 cites W1942214720 @default.
• W2479766063 cites W1944636972 @default.
• W2479766063 cites W1964105404 @default.
• W2479766063 cites W1965540688 @default.
• W2479766063 cites W1967254420 @default.
• W2479766063 cites W1968644258 @default.
• W2479766063 cites W1968765389 @default.
• W2479766063 cites W1969221769 @default.
• W2479766063 cites W1971726791 @default.
• W2479766063 cites W1972090215 @default.
• W2479766063 cites W1973349116 @default.
• W2479766063 cites W1975195907 @default.
• W2479766063 cites W1977707442 @default.
• W2479766063 cites W1978567855 @default.
• W2479766063 cites W1979187171 @default.
• W2479766063 cites W1979637090 @default.
• W2479766063 cites W1980871955 @default.
• W2479766063 cites W1980898129 @default.
• W2479766063 cites W1981089442 @default.
• W2479766063 cites W1982009503 @default.
• W2479766063 cites W1982360877 @default.
• W2479766063 cites W1982971733 @default.
• W2479766063 cites W1983506599 @default.
• W2479766063 cites W1985835804 @default.
• W2479766063 cites W1987213099 @default.
• W2479766063 cites W1988178270 @default.
• W2479766063 cites W1988448864 @default.
• W2479766063 cites W1991747510 @default.
• W2479766063 cites W1993144090 @default.
• W2479766063 cites W1994137684 @default.
• W2479766063 cites W1994318934 @default.
• W2479766063 cites W1996877429 @default.
• W2479766063 cites W1997183854 @default.
• W2479766063 cites W1998512969 @default.
• W2479766063 cites W1998952769 @default.
• W2479766063 cites W2000383699 @default.
• W2479766063 cites W2001514098 @default.
• W2479766063 cites W2005715606 @default.
• W2479766063 cites W2007168419 @default.
• W2479766063 cites W2010008722 @default.
• W2479766063 cites W2010763948 @default.
• W2479766063 cites W2014282903 @default.
• W2479766063 cites W2017550427 @default.
• W2479766063 cites W2018412575 @default.
• W2479766063 cites W2021096035 @default.
• W2479766063 cites W2021675347 @default.
• W2479766063 cites W2022088799 @default.
• W2479766063 cites W2022134547 @default.
• W2479766063 cites W2022194054 @default.
• W2479766063 cites W2024870937 @default.
• W2479766063 cites W2027895608 @default.
• W2479766063 cites W2028276939 @default.
• W2479766063 cites W2033369565 @default.
• W2479766063 cites W2034078038 @default.
• W2479766063 cites W2035491291 @default.
• W2479766063 cites W2035793410 @default.
• W2479766063 cites W2035865404 @default.
• W2479766063 cites W2036066742 @default.
• W2479766063 cites W2037045595 @default.
• W2479766063 cites W2038462265 @default.
• W2479766063 cites W2039386747 @default.
• W2479766063 cites W2040997459 @default.
• W2479766063 cites W2042751159 @default.
• W2479766063 cites W2046195371 @default.
• W2479766063 cites W2046510503 @default.
• W2479766063 cites W2048077351 @default.
• W2479766063 cites W2048795083 @default.
• W2479766063 cites W2050432652 @default.
• W2479766063 cites W2050776541 @default.
• W2479766063 cites W2051555499 @default.
• W2479766063 cites W2052853635 @default.
• W2479766063 cites W2054479383 @default.
• W2479766063 cites W2057772007 @default.
• W2479766063 cites W2058788374 @default.
• W2479766063 cites W2060795305 @default.
• W2479766063 cites W2061254824 @default.
• W2479766063 cites W2061497413 @default.
• W2479766063 cites W2063792498 @default.

• next