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CMS A long noncoding RNA regulates photoperiod-sensitive male sterility, an essential component of hybrid rice(2012) doi: 10.1073/pnas.1121374109 A non-coding RNA locus mediates environment-conditioned male sterility in rice. (2012) Cell Research 22:791–792. doi:10.1038/cr.2012.43 Comparative expression profiling of miRNA during anther development in genetic male sterile and wild type cotton. (2013) BMC Plant Biology 13:66 Differential Proteomic Analysis of Anthers between Cytoplasmic Male Sterile and Maintainer Lines in Capsicum annuum L.(2013) Int. J. Mol. Sci. 14(11), 22982-22996; doi:10.3390/ijms141122982 Transcriptome map of plant mitochondria reveals islands of unexpected transcribed regions (2011) BMC Genomics 12: 279. Heterozygous alleles restore male fertility to cytoplasmic male-sterile radish (Raphanus sativus L.): a case of overdominance(2013) J. Exp. Bot. 64: 2041-2048. Aging Genome 1. DNA damage 2. Epigenetic shifts 3. Telomere shortening Cellular level 1. Mitochondria: ROS, DNA damage, other 2. Misfolded proteins 3. Dysfunctional stem cells Organismal level 1. Autoimmune, other defects in immune system 2. Defective signaling Apoptosis Two basic steps: commitment and execution Commitment depends on interplay between various signals Bax & Bcl2 have opposite effects 2 main pathways: extrinsic & intrinsic Procaspase 8 binds FADD Procaspase 8 is processed to caspase 8 = initiator caspase Caspase 8 converts procaspase 3 to active form = executioner Caspase-3 & CAD execute the cell Intrinsic pathway Usually Bcl-2 protects mito Intracellular damage activates Bad or Bax Apoptosis Usually Bcl-2 protects mito Intracellular damage activates Bad or Bax Bad/Bax releases cyt c & AIF Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome Apoptosome processes procaspase -9 to caspase-9 = initiator caspase Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome Apoptosome processes procaspase -9 to caspase-9 = initiator caspase Caspase-9 converts caspase 3 to active form = executioner Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome Apoptosome processes procaspase -9 to caspase-9 = initiator caspase Caspase-9 converts caspase 3 to active form = executioner Caspase 3 & CAD execute the cell Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF AIF induces CAD Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF AIF induces CAD Destroys DNA Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF AIF induces CAD Destroys DNA Flips PS outside Apoptosis Intracellular damage activates Bad/Bax Bad/Bax release cyt c & AIF AIF induces CAD Destroys DNA Flips PS outside Phagocytic cells eat vesicles with external PS Apoptosis Two basic steps: commitment and execution Commitment depends on interplay between various signals TNF often stimulates recovery instead! Apoptosis in immunity PD1 receptor on T cells blocks apoptosis Binds PDL1 or PDL2 presented by other cells, including tumors Apoptosis in immunity PD1 receptor on T cells blocks apoptosis Binds PDL1 or PDL2 presented by other cells, including tumors PDL1 inhibitors are a new class of cancer drug Autophagy •Intracellular recycling process – lysosomes (animals); vacuoles (plants) Autophagy •Intracellular recycling process – lysosomes (animals); vacuoles (plants) •Removes misfolded proteins, bad organelles, intracell pathogens Autophagy •Intracellular recycling process – lysosomes (animals); vacuoles (plants) •Removes misfolded proteins, bad organelles, intracell pathogens •Promotes survival! Autophagy •Intracellular recycling process – lysosomes (animals); vacuoles (plants) •Removes misfolded proteins, bad organelles, intracell pathogens •Promotes survival! Reallocates nutrients to vital processes! Autophagy • Removes misfolded proteins, bad organelles, intracell pathogens • Promotes survival! Reallocates nutrients to vital processes! • Best way to get rid of bad mito w/o killing cell! • • • • Autophagy Removes misfolded proteins, bad organelles, intracell pathogens Promotes survival! Reallocates nutrients to vital processes! Best way to get rid of bad mito w/o killing cell! Associated with increased longevity in caloric restriction Autophagy • Associated with increased longevity in caloric restriction • Upregulated upon nutrient or growth factor deprivation Autophagy •Associated with increased longevity in caloric restriction •Upregulated upon nutrient or growth factor deprivation •Triggers PCD distinct from apoptosis if can’t cope • No caspase or CAD, chromatin laddering • Occurs inside lysosomes Autophagy •Triggers PCD distinct from apoptosis if can’t cope • No caspase or CAD, chromatin laddering • Occurs inside lysosomes •Highly regulated! Autophagy •Triggers PCD distinct from apoptosis if can’t cope • No caspase or CAD, chromatin laddering • Occurs inside lysosomes •Highly regulated! •Mis-regulation associated with heart disease, diabetes and many more Pyroptosis PCD associated with antimicrobial responses in inflammation Pyroptosis PCD associated with antimicrobial responses in inflammation Toll-like receptors bind PAMPs, eg bacterial flagellins Pyroptosis PCD associated with antimicrobial responses in inflammation Toll-like receptors bind PAMPs, eg bacterial flagellins Activated NOD-like receptors (NLRs) initiate assembly of pyroptosome Pyroptosis PCD associated with antimicrobial responses in inflammation Toll-like receptors bind PAMPs, eg bacterial flagellins Activated NOD-like receptors (NLRs) initiate assembly of pyroptosome Pyroptosome activates Caspase-1 Pyroptosis PCD associated with antimicrobial responses in inflammation Toll-like receptors bind PAMPs, eg bacterial flagellins Activated NOD-like receptors (NLRs) initiate assembly of pyroptosome Pyroptosome activates Caspase-1 Caspase-1 executes cell, Releasing PAMPs and cytokines Pyroptosis PCD associated with antimicrobial responses in inflammation Toll-like receptors bind PAMPs, eg bacterial flagellins Activated NOD-like receptors (NLRs) initiate assembly of pyroptosome Pyroptosome activates Caspase-1 Caspase-1 executes cell, Releasing PAMPs and Cytokines Reason for depletion of CD4 cells in AIDS Necroptosis PCD associated with viral infections Necroptosis PCD associated with viral infections Infected cells release TNF Necroptosis PCD associated with viral infections Infected cells release TNF TNFR activates RIPK1 RIPK1 binds RIPK3 to form necrosome Necroptosis PCD associated with viral infections Infected cells release TNF TNFR activates RIPK1 RIPK1 binds RIPK3 to form necrosome Necrosome activates MLKL which permeabilizes membranes Necroptosis vs apoptosis Tend to inhibit each other, but do have overlap Necroptosis vs apoptosis Tend to inhibit each other, but do have overlap Fail-safe for viruses that block apoptosis Ferroptosis PCD dependent on intra-cellular iron Triggered by inhibition of cystine uptake Ferroptosis PCD dependent on intra-cellular iron Triggered by inhibition of cystine uptake Reduced cystine uptake leads to the production of lethal lipid ROS Ferroptosis PCD dependent on intra-cellular iron Triggered by inhibition of cystine uptake Reduced cystine uptake leads to the production of lethal lipid ROS Erastin etc trigger it Ferroptosis PCD dependent on intra-cellular iron Triggered by inhibition of cystine uptake Reduced cystine uptake leads to the production of lethal lipid ROS Erastin etc trigger it Ferrostatin blocks it Autophagy – Plant PCD • Changes in shape and position of mitochondria (Mitochondrial morphology transition, MMT) • Nuclear condensation • Condensation of PM from cell wall • Deregulated: dev’l defects, lethality MMT (Scott & Logan, 2008, Plant Signaling & Behavior) Plant PCD In vegetative development – Suspensor degradation during embryo devt – Root cap devt and aerenchyma formation – Shaping of leaves Kawashima & Goldberg, 2009 PCD : Patterning in the lace plant leaf http://www.youtube.com/watch?v=9gis4HK1XPg http://completeaquarium.blogspot.com/2008/04/aponogeton-madagascariensis-lace-plant.html PCD: aerenchyma formation • Aerenchyma – – – – Tissue for gas exchange Aquatic species Induced by submergence Constitutive in rice: adaptation to flooding visible in all rice root types, except in small lateral roots Rebouillat et al., Rice 2009 Plant PCD • In vegetative development – Tracheary element formation PCD-specific hydrolytic enzymes accumulate in vacuole S1-nuclease cysteine proteases Vacuole enlarges bursts releases enzymes autolysis of cell contents & part of cw Plant PCD • In reproductive development – – – – Tapetum and stomium degradation in anther Female gametophyte devt Flower senescence Incompatibility reactions Model for integration of cytoskeletal events triggered by SI Poulter, N. S., et al. Plant Physiol. 2008;146:1358-1367 Copyright ©2008 American Society of Plant Biologists PCD : Evolutionary perspective Developed independently? Or evolved from a common ancestral cell death process? Some mol. components -- conserved e.g., PARP1, Bax-inhibitor-1, Defender against Apoptotic Death-1 http://bifi.unizar.es/research/pro_pro_inter_elec_transfer/research.php PCD : Evolutionary perspective • Caspases – Cysteine proteases – Mol switches that activate c death • Plants have proteases w/ caspase-like activities : • Vacuolar processing enzymes (VPEs) Gao et al., Plant Signaling & Behav. 2008 PCD : role of mitochondrion Mitochondria -sensor of death signals & initiator of biochem processes leading to cell death http://bifi.unizar.es/research/pro_pro_inter_elec_transfer/research.php PCD : a role for chloroplasts PCD occurs independently of chloroplasts • Chloroplasts – determine severity of & number of cells undergoing AL-PCD – ROS • Elevated levels – physiological damage • Signaling mol. Gao et al., Plant Signaling & Behav. 2008 Cell death due to biotic/abiotic stress Abiotic stresses: Temperature extremes Ozone Hypoxia Mediated by plant hormones Ethylene Jasmonic acid Salicylic acid Regulators: Reactive oxygen species (ROS): Superoxide anion radical Hydrogen peroxide (H2O2) Nitric oxide (NO) Steffens and Sauter, Plant Cell, 2009