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Academic literature on the topic 'Peroxisomes'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 May 2024

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Journal articles on the topic "Peroxisomes"

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Somborac, Tamara, Güleycan Lutfullahoglu Bal, Kaneez Fatima, Helena Vihinen, Anja Paatero, Eija Jokitalo, Ville O. Paavilainen, and Svetlana Konovalova. "The subset of peroxisomal tail-anchored proteins do not reach peroxisomes via ER, instead mitochondria can be involved." PLOS ONE 18, no. 12 (December 1, 2023): e0295047. http://dx.doi.org/10.1371/journal.pone.0295047.

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Peroxisomes are membrane-enclosed organelles with important roles in fatty acid breakdown, bile acid synthesis and biosynthesis of sterols and ether lipids. Defects in peroxisomes result in severe genetic diseases, such as Zellweger syndrome and neonatal adrenoleukodystrophy. However, many aspects of peroxisomal biogenesis are not well understood. Here we investigated delivery of tail-anchored (TA) proteins to peroxisomes in mammalian cells. Using glycosylation assays we showed that peroxisomal TA proteins do not enter the endoplasmic reticulum (ER) in both wild type (WT) and peroxisome-lacking cells. We observed that in cells lacking the essential peroxisome biogenesis factor, PEX19, peroxisomal TA proteins localize mainly to mitochondria. Finally, to investigate peroxisomal TA protein targeting in cells with fully functional peroxisomes we used a proximity biotinylation approach. We showed that while ER-targeted TA construct was exclusively inserted into the ER, peroxisome-targeted TA construct was inserted to both peroxisomes and mitochondria. Thus, in contrast to previous studies, our data suggest that some peroxisomal TA proteins do not insert to the ER prior to their delivery to peroxisomes, instead, mitochondria can be involved.

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South, Sarah T., and Stephen J. Gould. "Peroxisome Synthesis in the Absence of Preexisting Peroxisomes." Journal of Cell Biology 144, no. 2 (January 25, 1999): 255–66. http://dx.doi.org/10.1083/jcb.144.2.255.

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Zellweger syndrome and related diseases are caused by defective import of peroxisomal matrix proteins. In all previously reported Zellweger syndrome cell lines the defect could be assigned to the matrix protein import pathway since peroxisome membranes were present, and import of integral peroxisomal membrane proteins was normal. However, we report here a Zellweger syndrome patient (PBD061) with an unusual cellular phenotype, an inability to import peroxisomal membrane proteins. We also identified human PEX16, a novel integral peroxisomal membrane protein, and found that PBD061 had inactivating mutations in the PEX16 gene. Previous studies have suggested that peroxisomes arise from preexisting peroxisomes but we find that expression of PEX16 restores the formation of new peroxisomes in PBD061 cells. Peroxisome synthesis and peroxisomal membrane protein import could be detected within 2–3 h of PEX16 injection and was followed by matrix protein import. These results demonstrate that peroxisomes do not necessarily arise from division of preexisting peroxisomes. We propose that peroxisomes may form by either of two pathways: one that involves PEX11-mediated division of preexisting peroxisomes, and another that involves PEX16-mediated formation of peroxisomes in the absence of preexisting peroxisomes.

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Voorn-Brouwer, Tineke, Astrid Kragt, Henk F. Tabak, and Ben Distel. "Peroxisomal membrane proteins are properly targeted to peroxisomes in the absence of COPI- and COPII-mediated vesicular transport." Journal of Cell Science 114, no. 11 (June 1, 2001): 2199–204. http://dx.doi.org/10.1242/jcs.114.11.2199.

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The classic model for peroxisome biogenesis states that new peroxisomes arise by the fission of pre-existing ones and that peroxisomal matrix and membrane proteins are recruited directly from the cytosol. Recent studies challenge this model and suggest that some peroxisomal membrane proteins might traffic via the endoplasmic reticulum to peroxisomes. We have studied the trafficking in human fibroblasts of three peroxisomal membrane proteins, Pex2p, Pex3p and Pex16p, all of which have been suggested to transit the endoplasmic reticulum before arriving in peroxisomes. Here, we show that targeting of these peroxisomal membrane proteins is not affected by inhibitors of COPI and COPII that block vesicle transport in the early secretory pathway. Moreover, we have obtained no evidence for the presence of these peroxisomal membrane proteins in compartments other than peroxisomes and demonstrate that COPI and COPII inhibitors do not affect peroxisome morphology or integrity. Together, these data fail to provide any evidence for a role of the endoplasmic reticulum in peroxisome biogenesis.

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Bascom, Roger A., Honey Chan, and Richard A. Rachubinski. "Peroxisome Biogenesis Occurs in an Unsynchronized Manner in Close Association with the Endoplasmic Reticulum in Temperature-sensitiveYarrowia lipolyticaPex3p Mutants." Molecular Biology of the Cell 14, no. 3 (March 2003): 939–57. http://dx.doi.org/10.1091/mbc.e02-10-0633.

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Pex3p is a peroxisomal integral membrane protein required early in peroxisome biogenesis, and Pex3p-deficient cells lack identifiable peroxisomes. Two temperature-sensitive pex3 mutant strains of the yeast Yarrowia lipolytica were made to investigate the role of Pex3p in the early stages of peroxisome biogenesis. In glucose medium at 16°C, these mutants underwent de novo peroxisome biogenesis and exhibited early matrix protein sequestration into peroxisome-like structures found at the endoplasmic reticulum-rich periphery of cells or sometimes associated with nuclei. The de novo peroxisome biogenesis seemed unsynchronized, with peroxisomes occurring at different stages of development both within cells and between cells. Cells with peripheral nascent peroxisomes and cells with structures morphologically distinct from peroxisomes, such as semi/circular tubular structures that immunostained with antibodies to peroxisomal matrix proteins and to the endoplasmic reticulum-resident protein Kar2p, and that surrounded lipid droplets, were observed during up-regulation of peroxisome biogenesis in cells incubated in oleic acid medium at 16°C. These structures were not detected in wild-type or Pex3p-deficient cells. Their role in peroxisome biogenesis remains unclear. Targeting of peroxisomal matrix proteins to these structures suggests that Pex3p directly or indirectly sequesters components of the peroxisome biogenesis machinery. Such a role is consistent with Pex3p overexpression producing cells with fewer, larger, and clustered peroxisomes.

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Singin, Öznur, Artur Astapenka, Victor Costina, Sandra Kühl, Nina Bonekamp, Oliver Drews, and Markus Islinger. "Analysis of the Mouse Hepatic Peroxisome Proteome—Identification of Novel Protein Constituents Using a Semi-Quantitative SWATH-MS Approach." Cells 13, no. 2 (January 17, 2024): 176. http://dx.doi.org/10.3390/cells13020176.

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Ongoing technical and bioinformatics improvements in mass spectrometry (MS) allow for the identifying and quantifying of the enrichment of increasingly less-abundant proteins in individual fractions. Accordingly, this study reassessed the proteome of mouse liver peroxisomes by the parallel isolation of peroxisomes from a mitochondria- and a microsome-enriched prefraction, combining density-gradient centrifugation with a semi-quantitative SWATH-MS proteomics approach to unveil novel peroxisomal or peroxisome-associated proteins. In total, 1071 proteins were identified using MS and assessed in terms of their distribution in either high-density peroxisomal or low-density gradient fractions, containing the bulk of organelle material. Combining the data from both fractionation approaches allowed for the identification of specific protein profiles characteristic of mitochondria, the ER and peroxisomes. Among the proteins significantly enriched in the peroxisomal cluster were several novel peroxisomal candidates. Five of those were validated by colocalization in peroxisomes, using confocal microscopy. The peroxisomal import of HTATIP2 and PAFAH2, which contain a peroxisome-targeting sequence 1 (PTS1), could be confirmed by overexpression in HepG2 cells. The candidates SAR1B and PDCD6, which are known ER-exit-site proteins, did not directly colocalize with peroxisomes, but resided at ER sites, which frequently surrounded peroxisomes. Hence, both proteins might concentrate at presumably co-purified peroxisome-ER membrane contacts. Intriguingly, the fifth candidate, OCIA domain-containing protein 1, was previously described as decreasing mitochondrial network formation. In this work, we confirmed its peroxisomal localization and further observed a reduction in peroxisome numbers in response to OCIAD1 overexpression. Hence, OCIAD1 appears to be a novel protein, which has an impact on both mitochondrial and peroxisomal maintenance.

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Kim, Jung-Ae. "Peroxisome Metabolism in Cancer." Cells 9, no. 7 (July 14, 2020): 1692. http://dx.doi.org/10.3390/cells9071692.

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Peroxisomes are metabolic organelles involved in lipid metabolism and cellular redoxbalance. Peroxisomal function is central to fatty acid oxidation, ether phospholipid synthesis, bile acidsynthesis, and reactive oxygen species homeostasis. Human disorders caused by genetic mutations inperoxisome genes have led to extensive studies on peroxisome biology. Peroxisomal defects are linkedto metabolic dysregulation in diverse human diseases, such as neurodegeneration and age-relateddisorders, revealing the significance of peroxisome metabolism in human health. Cancer is a diseasewith metabolic aberrations. Despite the critical role of peroxisomes in cell metabolism, the functionaleects of peroxisomes in cancer are not as well recognized as those of other metabolic organelles,such as mitochondria. In addition, the significance of peroxisomes in cancer is less appreciated thanit is in degenerative diseases. In this review, I summarize the metabolic pathways in peroxisomesand the dysregulation of peroxisome metabolism in cancer. In addition, I discuss the potential ofinactivating peroxisomes to target cancer metabolism, which may pave the way for more eectivecancer treatment.

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Heyman, J. A., E. Monosov, and S. Subramani. "Role of the PAS1 gene of Pichia pastoris in peroxisome biogenesis." Journal of Cell Biology 127, no. 5 (December 1, 1994): 1259–73. http://dx.doi.org/10.1083/jcb.127.5.1259.

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Several groups have reported the cloning and sequencing of genes involved in the biogenesis of yeast peroxisomes. Yeast strains bearing mutations in these genes are unable to grow on carbon sources whose metabolism requires peroxisomes, and these strains lack morphologically normal peroxisomes. We report the cloning of Pichia pastoris PAS1, the homologue (based on a high level of protein sequence similarity) of the Saccharomyces cerevisiae PAS1. We also describe the creation and characterization of P. pastoris pas1 strains. Electron microscopy on the P. pastoris pas1 cells revealed that they lack morphologically normal peroxisomes, and instead contain membrane-bound structures that appear to be small, mutant peroxisomes, or "peroxisome ghosts." These "ghosts" proliferated in response to induction on peroxisome-requiring carbon sources (oleic acid and methanol), and they were distributed to daughter cells. Biochemical analysis of cell lysates revealed that peroxisomal proteins are induced normally in pas1 cells. Peroxisome ghosts from pas1 cells were purified on sucrose gradients, and biochemical analysis showed that these ghosts, while lacking several peroxisomal proteins, did import varying amounts of several other peroxisomal proteins. The existence of detectable peroxisome ghosts in P. pastoris pas1 cells, and their ability to import some proteins, stands in contrast with the results reported by Erdmann et al. (1991) for the S. cerevisiae pas1 mutant, in which they were unable to detect peroxisome-like structures. We discuss the role of PAS1 in peroxisome biogenesis in light of the new information regarding peroxisome ghosts in pas1 cells.

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Hoepfner, Dominic, Marlene van den Berg, Peter Philippsen, Henk F. Tabak, and Ewald H. Hettema. "A role for Vps1p, actin, and the Myo2p motor in peroxisome abundance and inheritance in Saccharomyces cerevisiae." Journal of Cell Biology 155, no. 6 (December 3, 2001): 979–90. http://dx.doi.org/10.1083/jcb.200107028.

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In vivo time-lapse microscopy reveals that the number of peroxisomes in Saccharomyces cerevisiae cells is fairly constant and that a subset of the organelles are targeted and segregated to the bud in a highly ordered, vectorial process. The dynamin-like protein Vps1p controls the number of peroxisomes, since in a vps1Δ mutant only one or two giant peroxisomes remain. Analogous to the function of other dynamin-related proteins, Vps1p may be involved in a membrane fission event that is required for the regulation of peroxisome abundance. We found that efficient segregation of peroxisomes from mother to bud is dependent on the actin cytoskeleton, and active movement of peroxisomes along actin filaments is driven by the class V myosin motor protein, Myo2p: (a) peroxisomal dynamics always paralleled the polarity of the actin cytoskeleton, (b) double labeling of peroxisomes and actin cables revealed a close association between both, (c) depolymerization of the actin cytoskeleton abolished all peroxisomal movements, and (d) in cells containing thermosensitive alleles of MYO2, all peroxisome movement immediately stopped at the nonpermissive temperature. In addition, time-lapse videos showing peroxisome movement in wild-type and vps1Δ cells suggest the existence of various levels of control involved in the partitioning of peroxisomes.

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Fagarasanu, Monica, Andrei Fagarasanu, Yuen Yi C. Tam, John D. Aitchison, and Richard A. Rachubinski. "Inp1p is a peroxisomal membrane protein required for peroxisome inheritance in Saccharomyces cerevisiae." Journal of Cell Biology 169, no. 5 (May 31, 2005): 765–75. http://dx.doi.org/10.1083/jcb.200503083.

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Cells have evolved molecular mechanisms for the efficient transmission of organelles during cell division. Little is known about how peroxisomes are inherited. Inp1p is a peripheral membrane protein of peroxisomes of Saccharomyces cerevisiae that affects both the morphology of peroxisomes and their partitioning during cell division. In vivo 4-dimensional video microscopy showed an inability of mother cells to retain a subset of peroxisomes in dividing cells lacking the INP1 gene, whereas cells overexpressing INP1 exhibited immobilized peroxisomes that failed to be partitioned to the bud. Overproduced Inp1p localized to both peroxisomes and the cell cortex, supporting an interaction of Inp1p with specific structures lining the cell periphery. The levels of Inp1p vary with the cell cycle. Inp1p binds Pex25p, Pex30p, and Vps1p, which have been implicated in controlling peroxisome division. Our findings are consistent with Inp1p acting as a factor that retains peroxisomes in cells and controls peroxisome division. Inp1p is the first peroxisomal protein directly implicated in peroxisome inheritance.

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Kim, Peter K., Robert T. Mullen, Uwe Schumann, and Jennifer Lippincott-Schwartz. "The origin and maintenance of mammalian peroxisomes involves a de novo PEX16-dependent pathway from the ER." Journal of Cell Biology 173, no. 4 (May 22, 2006): 521–32. http://dx.doi.org/10.1083/jcb.200601036.

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Peroxisomes are ubiquitous organelles that proliferate under different physiological conditions and can form de novo in cells that lack them. The endoplasmic reticulum (ER) has been shown to be the source of peroxisomes in yeast and plant cells. It remains unclear, however, whether the ER has a similar role in mammalian cells and whether peroxisome division or outgrowth from the ER maintains peroxisomes in growing cells. We use a new in cellula pulse-chase imaging protocol with photoactivatable GFP to investigate the mechanism underlying the biogenesis of mammalian peroxisomes. We provide direct evidence that peroxisomes can arise de novo from the ER in both normal and peroxisome-less mutant cells. We further show that PEX16 regulates this process by being cotranslationally inserted into the ER and serving to recruit other peroxisomal membrane proteins to membranes. Finally, we demonstrate that the increase in peroxisome number in growing wild-type cells results primarily from new peroxisomes derived from the ER rather than by division of preexisting peroxisomes.

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Dissertations / Theses on the topic "Peroxisomes"

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Karnati, Srikanth. "Functional characterization of peroxisomes and pathological consequences of peroxisomal dysfunction in the lung." Giessen : VVB Lauferweiler, 2009. http://d-nb.info/100020572X/04.

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Castro, Ines Gomes Oliveira. "Tail-anchored proteins at peroxisomes : identification of MIRO1 as a novel peroxisomal motility factor." Thesis, University of Exeter, 2016. http://hdl.handle.net/10871/24657.

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Peroxisomes are dynamic and multifunctional organelles, which are essential for human health and development. They are remarkably diverse, with functions that vary significantly between cells and organisms, and can dramatically change their size, shape and dynamics in response to cellular cues. In the past few years, several studies have significantly increased our understanding of the basic principles that enable peroxisome biogenesis and degradation, as well as their pivotal role in cellular signalling and homeostasis. However, several of these processes are still poorly understood. In this thesis we initially studied the peroxisome targeting mechanism of a group of C-terminally anchored membrane proteins, known as tail-anchored (TA) proteins. In order to investigate the molecular signals that enable TA protein targeting to cellular organelles, we analysed the physicochemical properties of a cohort of TA proteins both in silico and in vivo, and show that a combination of transmembrane domain (TMD) hydrophobicity and C-terminal tail charge determines organelle-specific targeting. Focusing on peroxisomes, we demonstrate that a balance between TMD hydrophobicity and high positive tail charge directs TA proteins to this organelle, and enables binding to the peroxisomal chaperone PEX19. These results allowed us to create a bioinformatical tool to predict the targeting of uncharacterised TA proteins and further develop our understanding of the molecular mechanisms involved in the targeting of this protein group. From our initial TA protein screen, we identified the TA protein MIRO1 at peroxisomes and looked at its role in the regulation of peroxisome motility. We show that endogenous MIRO1 localises to mitochondria and peroxisomes, and that dual targeting depends on the C-terminal tail. MIRO1 expression significantly increased peroxisome motility in several cell lines, and revealed a role for motility in peroxisome dynamics, by inducing organelle proliferation and elongation. These results reveal a new molecular complex at peroxisomes and provide us with a tool to further dissect the role of motility on peroxisome function.

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Liu, Xiaoxi. "BEYOND PEROXISOME: ABCD2 MODIFIES PPARα SIGNALING AND IDENTIFIES A SUBCLASS OF PEROXISOMES IN MOUSE ADIPOSE TISSUE." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/41.

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ABCD2 (D2) has been proposed as a peroxisomal long-chain acyl-CoA transporter that is essential for very long chain fatty acid metabolism. In the livers of mice, D2 is highly induced by fenofibrate, a PPARα ligand that has been widely used as a lipid lowering agent in the treatment of hypertriglyceridemia. To determine if D2 is a modifier of fibrate responses, wild-type and D2 deficient mice were treated with fenofibrate for 14 days. The absence of D2 altered expression of gene clusters associated with lipid metabolism, including PPARα signaling. Using 3T3-L1 adipocytes, which express high levels of D2, we confirmed that knock-down of D2 modified genomic responses to fibrate treatment. We next evaluated the impact of D2 on effects of fibrates in a mouse model of dietinduced obesity. Fenofibrate treatment opposed the development of obesity, hypertriglyceridemia, and insulin resistance. However, these effects were unaffected by D2 genotype. We concluded that D2 can modulate genomic responses to fibrates, but that these effects are not sufficiently robust to alter the effects of fibrates on diet-induced obesity phenotypes. Although proposed as a peroxisomal transporter, the intracellular localization of D2, especially in adipose tissue, has not been validated with direct experimental evidence. Sequential centrifugation of mouse adipose homogenates generated a fraction enriched with D2, but lacked well-known peroxisome markers including catalase, PEX19, and ABCD3 (D3). Electron microscopic imaging of this fraction confirmed the presence of D2 protein on an organelle with evidence of a dense matrix and a diameter of ~200 nm, the typical structure and size of a microperoxisome. D2 and PEX19 antibodies recognized distinct structures in mouse adipose. Immunoisolation of the D2-containing compartment from adipose tissue confirmed the scarcity of PEX19. Proteomic profiling of the D2 compartment revealed the presence of proteins associated peroxisome, endoplasmic reticulum (ER), and mitochondria. We conclude that D2 is localized to a distinct subclass of peroxisomes that lack many peroxisome proteins and may physically associate with mitochondria and the ER.

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Aboushadi, Nahla Mohamed. "Role of peroxisomes in isoprenoid biosynthesis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9963646.

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Karnati, Srikanth [Verfasser]. "Functional characterization of peroxisomes and pathological consequences of peroxisomal dysfunction in the lung / by Srikanth Karnati." Giessen : VVB Laufersweiler, 2009. http://d-nb.info/999686674/34.

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Bottger, Gina. "Receptor-mediated import of proteins into peroxisomes." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/60502.

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Vries, Bart de. "The biology of peroxisomes in Hansenula polymorpha." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn.

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Anderson, I. W. "Permeability of leaf peroxisomes to photorespiratory metabolites." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379882.

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Drago, Ilaria. "Ca2+ homeostasis in mammalian and plant peroxisomes." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426033.

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Peroxisomes are single-membrane bound organelles involved in reactive oxygen species scavenging, ?- and ?-oxidation of fatty acids, biosynthesis of ether phospholipids and other metabolic pathways. Although recent studies have highlighted the mechanisms of peroxisomal formation, fusion-fission, protein import etc. little information is available concerning a possible role of peroxisomes in cellular signalling, and, until very recently, no information was available about a possible role of peroxisomes in cellular Ca2+ handling. Ca2+ signalling exerts a plethora of functions in cells (both in physiology and pathology) and while the role of subcellular compartments like endoplasmic reticulum, mitochondria, nucleus and Golgi apparatus in Ca2+ handling has been intensively investigated in the last decades, peroxisomes remained a black whole in the picture. Last, but not least, a renewed interest towards peroxisome functions has been triggered by the discovery of a number of human diseases (called “peroxisomal disorders”) that are due to mutations of peroxisomal proteins. For all these reasons, I decided to investigate if and how peroxisomes play a role in cellular Ca2+ handling. I targeted a genetically encoded, FRET-based Ca2+ sensor to peroxisomal matrix and I found that the Ca2+ concentration of peroxisomes in living cells at rest is similar to that of the cytosol, while increases in cytosolic Ca2+ concentration (elicited by either Ca2+ mobilization from stores or Ca2+ influx through plasma membrane Ca2+ channels) are usually followed by a slow rise in intraperoxisomal Ca2+ concentration. I also investigated the mechanism of peroxisomal Ca2+ entry and I found that Ca2+ influx into peroxisomes is not driven by an ATP-dependent pump, membrane potential or H+ (Na+) gradients. However, the peroxisomal membrane appears to play a low-pass filter role, preventing the organelle from taking up Ca2+ during short lasting cytosolic Ca2+ transients, while allowing equilibration of the peroxisomal luminal Ca2+ concentration with that of the cytosol during prolonged cytosolic Ca2+ increases. Thus, peroxisomes appear to be an additional cytosolic Ca2+ buffer, but their influx and efflux mechanisms are unlike those of any other cellular organelle. The second part of my work was aimed at understanding the physiological function of this phenomenon. To date, no Ca2+-regulated mammalian peroxisomal enzyme is known. On the contrary, there are some Ca2+-regulated plant peroxisomal enzymes, in particular an isoform of the H2O2 scavenging enzyme catalase, Cat3. Cat3 has been shown to be specifically located in plant peroxisomes and to be activated in vitro by Ca2+ and calmodulin. The peroxisomal Ca2+ probe employed in the first part of this work was expressed in plant peroxisomes and revealed that the phenomenon of Ca2+ entry into peroxisomal matrix in plants is very similar, both in amplitude and kinetic, to that of mammalian cells. Plasma membrane hyperpolarization demonstrated to be a reliable stimulus to trigger a prolonged rise of peroxisomal (and cytosolic) Ca2+ concentration and so it was chosen in order to verify if a peroxisomal Ca2+ rise can somehow affect H2O2 scavenging. Preliminary experiments performed in Arabidopsis plants stably expressing in peroxisomes a H2O2 sensor indicate that H2O2 scavenging is accelerated by Ca2+ entry and this is correlated with the level of Cat3 within peroxisomes.
I perossisomi sono degli organelli intracellulari circondati da una singola membrana coinvolti nell’eliminazione di specie reattive dell’ossigeno, ?- e ?-ossidazione di acidi grassi, biosintesi di eteri di fosfolipidi e in altre reazioni metaboliche. Sebbene studi recenti abbiano elucidato i meccanismi alla base della formazione, della fusione- fissione e dell’importo di proteine nella matrice dei perossisomi, le informazioni riguardanti il ruolo dei perossisomi nel signalling cellulare sono scarse e, fino a poco tempo fa, quelle riguardanti il possibile ruolo dei perossisomi nel signalling cellulare del Ca2+ erano totalmente assenti. Il signalling del Ca2+ è alla base di un ampio numero di funzioni cellulari sia fisiologiche che patologiche e mentre il ruolo di compartimenti subcellulari come il reticolo endoplasmico, i mitocondri, il nucleo e l’apparato di Golgi nelle dinamiche intracellulari del Ca2+ è stato ampiamente studiato negli ultimi decenni, i perossisomi sono rimasti nella “zona d’ombra” di questo scenario. Infine, c’è stato ultimamente un rinnovato interesse circa le funzioni dei perossisomi grazie alla scoperta di un certo numero di malattie umane (chiamate “disordini dei perossisomi”) dovute a mutazioni di proteine perossisomiali. Per tutte queste ragioni, ho deciso di investigare se, e come, i perossisomi rivestono un qualche ruolo nell’omeostasi intracellulare del Ca2+. A questo scopo ho indirizzato alla matrice dei perossisomi una sonda per il Ca2+ geneticamente codificata e basata su FRET e ho potuto dimostrare che la concentrazione di Ca2+ nei perossisomi di cellule vive in condizioni di riposo è molto simile a quella citosolica mentre aumenti della concentrazione di Ca2+ (causati sia da mobilizzazione di Ca2+ dai depositi intracellulari che da influsso attraverso canali per il Ca2+ situati nella membrana plasmatica) sono solitamente seguiti da un lento aumento della concentrazione di Ca2+ nella matrice perossisomiale. Mi sono inoltre occupata della caratterizzazione del meccanismo che sta alla base dell’entrata di Ca2+ nei perossisomi e sono arrivata alla conclusione che questo fenomeno non è dovuto alla presenza di una pompa dipendente da ATP, né di un potenziale di membrana o di un gradiente di H+ o Na+. La membrana dei perossisomi sembra costituire una barriera che previene l’entrata di Ca2+ nel caso di aumenti brevi nel tempo, mentre nel caso di aumenti prolungati della concentrazione di Ca2+ nel citosol permette una lenta equilibrazione della concentrazione di Ca2+ nella matrice perossisomiale con l’ambiente citosolico. I perossisomi sembrano quindi costituire un nuovo sistema-tampone per il Ca2+del citosol, sebbene il loro meccanismo di influsso ed efflusso per il Ca2+ è totalmente differente da quello di ogni altro organello cellulare. La seconda parte del mio lavoro si è poi concentrata sullo studio dei possibili ruoli fisiologici del fenomeno dell’entrata di Ca2+ nei perossisomi. In letteratura non sono al momento riportati degli enzimi localizzati nei perossisomi delle cellule di mammifero che siano regolati da Ca2+; al contrario, alcuni enzimi localizzati nei perossisomi delle piante sembrano essere regolati da Ca2+. Di questi, quello che più mi è sembrato interessante è un’isoforma di un enzima deputato all’eliminazione di H2O2, la catalasi. L’attività di Cat3 è infatti riportata essere attivata in vitro da Ca2+ e calmodulina. La sonda per il Ca2+ utilizzata per lo studio dei perossisomi in cellule di mammifero è stata quindi indirizzata ai perossisomi di cellule vegetali e ha permesso di dimostrare che il fenomeno dell’entrata di Ca2+ nei perossisomi è molto simile, sia per ampiezza che per cinetica, tra perossisomi di mammifero e di pianta. L’iperpolarizzazione della membrana plasmatica ha dimostrato essere uno stimolo ripetibile che causa un prolungato aumento della concentrazione di Ca2+ nei perossisomi (e nel citosol) di pianta ed è quindi stato scelto per verificare se un aumento di Ca2+ nei perossisomi possa in qualche modo influenzare l’eliminazione di H2O2. Esperimenti preliminari effettuati in piante di Arabidopsis che esprimono stabilmente una sonda per H2O2 geneticamente codificata indicano che l’eliminazione di H2O2 è notevolmente accelerata in seguito all’entrata di Ca2+; questo correla con il livello di Cat3 espressa nei perossisomi.

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Smith, Jennifer Joy. "Maintenance of peroxisomes in the yeast Yarrowia lipolytica." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0008/NQ59670.pdf.

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Books on the topic "Peroxisomes"

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Schrader, Michael, ed. Peroxisomes. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6937-1.

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Latruffe, Norbert, and Maurice Bugaut, eds. Peroxisomes. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7.

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Norbert, Latruffe, and Bugaut M. 1945-, eds. Peroxisomes. Berlin: Springer-Verlag, 1994.

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Schrader, Michael, ed. Peroxisomes. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3048-8.

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Baker, Alison, and Ian A. Graham, eds. Plant Peroxisomes. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-015-9858-3.

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del Río, Luis A., and Michael Schrader, eds. Proteomics of Peroxisomes. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2233-4.

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K, Reddy Janardan, ed. Peroxisomes: Biology and role in toxicology and disease. New York, N.Y: New York Academy of Sciences, 1996.

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Roels, Frank. Peroxisomes: A personal account. Brussel: VUB Press, 1991.

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Fahimi, H. Dariush, and Helmut Sies, eds. Peroxisomes in Biology and Medicine. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71325-5.

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1933-, Fahimi H. Dariush, Sies H. 1942-, European Cell Biology Organization, and International Symposium on Peroxisomes in Biology and Medicine (1986 : Heidelberg, Germany), eds. Peroxisomes in biology and medicine. Berlin: Springer-Verlag, 1987.

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Book chapters on the topic "Peroxisomes"

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Valk, Jacob, and Marjo S. van der Knaap. "Peroxisomes and Peroxisomal Disorders." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 97–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_14.

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Wanders, R. J. A. "Peroxisomes and Peroxisomal Disorders." In Magnetic Resonance of Myelination and Myelin Disorders, 151–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27660-2_17.

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van der Knaap, Marjo S., and Jacob Valk. "Peroxisomes and Peroxisomal Disorders." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 106–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03078-3_14.

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Van Veldhoven, P. P., and A. Völkl. "General Indroduction to Isolation and Characterization of Peroxisomes." In Peroxisomes, 3–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_1.

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Goudonnet, H., J. Magdalou, and S. Fournel-Gigleux. "Measurement of the in Vitro Glucuronidation of Peroxisome Proliferator Carboxylic Acids by Liver Microsomes and Genetically Modified V79 Cell Line." In Peroxisomes, 151–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_10.

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Benmbarek, A. "Molecular Modeling and Drug Design: Application to Some Peroxisome Proliferator Agents." In Peroxisomes, 159–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_11.

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Brocard, C., L. C. Ramirez, and P. Bournot. "Fao Cell Line as a Model for the Study of the Effect of Peroxisome Proliferators on Cellular Functions." In Peroxisomes, 171–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_12.

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Causeret, C., M. Bentéjac, and M. Bugaut. "Measurement of Dihydroxyacetone-Phosphate Acyl-Transferase (DHAP-AT) Activity in Liver Peroxisomes and Cell Lines." In Peroxisomes, 181–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_13.

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Ng, K. H., E. B. Bioukar, F. Straehli, and J. Deschatrette. "In Vitro Transformation of Human Fibroblasts with SV40 T Antigen (Lipofection)." In Peroxisomes, 189–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_14.

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Bioukar, E. B., F. Straehli, K. H. Ng, and J. Deschatrette. "Somatic Cell Hybridization as a Tool for Genetic Analysis of Peroxisomal Activities." In Peroxisomes, 195–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87807-7_15.

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Conference papers on the topic "Peroxisomes"

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Sturk, A., M. C. L. Schaap, A. Prins Heymans, J. W. ten Cate, R. J. A. Wanders, H. S. A. Heymans, R. B. H. Schutgens, and H. van den Bosch. "SEVERELY IMPAIRED SYNTHESIS OF PLATELET ACTIVATING FACTOR IN CHONDRO DYSPLASIA PUNCTATA RHIZOMELIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642883.

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The first steps of the de novo synthesis of alkoxyether lipids, like plasmalogens and platelet activating factor (PAF) are localized in the peroxisome. We have previously reported the severely impaired PAF synthesis in Zellweger patients. These patients lack cytochemically detectable peroxisomes, and have a severely impaired alkoxyether lipid synthesis. However, chondro dysplasia punctata (CDP) patients have also been shown to have an impaired alkoxyether lipid synthesis. We therefore investigated PAF synthesis in CDP patients.Platelets and leucocytes were isolated from 3 CDP patients. Leucocytes from normal controls produced 4678 ± 2033 pMoles PAF/10 cells (n=6, range 1698-7058) when optimally stimulated with Ca2+-ionophore A23187. Normal control platelets produced 0.6 ± 0.3 pMoles PAF/10 cells (n=6, range 0.3-1.0) when optimally stimulated with thrombin. PAF synthesis by the leucocytes of the patients was severely reduced, but detectable. Leucocytes from patient 1, 2 and 3 synthesized 9, 660 and 325 pMoles PAF/10 cells respectively. Platelets from the patients 1, 2 and 3 synthesized 0.1, 0.2 and 0.2 pMoles PAF/10 cells respectively.Platelet aggregation, induced by ADP, PAF, or thrombin (also in the presence of inhibitors of the first and second pathway of platelet activation) was normal.We conclude that PAF synthesis is severely impaired in leucocytes and reduced in platelets from CDP patients. The residual platelet PAF synthesis may suffice to warrant normal platelet functioning.

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Niemisto, Antti, Jyrki Selinummi, Ramsey Saleem, Ilya Shmulevich, John Aitchison, and Olli Yli-Harja. "Extraction of the Number of Peroxisomes in Yeast Cells by Automated Image Analysis." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.259890.

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Niemisto, Antti, Jyrki Selinummi, Ramsey Saleem, Ilya Shmulevich, John Aitchison, and Olli Yli-Harja. "Extraction of the Number of Peroxisomes in Yeast Cells by Automated Image Analysis." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397915.

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Selinummi, J., A. Niemisto, R. Saleem, G. W. Carter, J. Aitchison, O. Yli-Harja, I. Shmulevich, and J. Boyle. "A Case Study on 3-D Reconstruction and Shape Description of Peroxisomes in Yeast." In 2007 IEEE International Conference on Signal Processing and Communications. IEEE, 2007. http://dx.doi.org/10.1109/icspc.2007.4728408.

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IMADA, I., EF SATO, R. KONAKA, M. NISHIKAWA, Y. KIRA, A.-M. PARK, Q. LI, and M. INOUE. "EFFECTS OF CALORIC RESTRICTION AND AGING ON THE GENERATION OF REACTIVE OXYGEN SPECIES IN RAT LIVER MITOCHONDRIA AND PEROXISOMES." In Proceedings of the 13th International Symposium. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702203_0069.

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Vasconcelos, Matheus Felipe de Souza, Francisco Tomaz Meneses de Oliveira, Rafael Zini Moreira da Silva, and Alex Michel Daoud. "Neurological and adrenal insufficiency symptons in adult x-linked adrenoleukodystrophy: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.347.

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Context: X-linked adrenoleukodystrophy (X-ALD) is a rare genetic demyelinating disease caused by mutations in ABC1 gen associated with an impairment of beta- oxidation of very long chain fatty acids (VLCFA) in peroxisomes. It causes accumulation of VCLFA in tissues affecting majoritary the central nervous system, testicles and the adrenal córtex resulting in symptoms which provides restricted neurological prognosis and sequels. Methods: Specific data related of a clinical case through prontuary and complementary exams in a patient attended at Santa Casa de Misericórdia de São Paulo hospital. Case report: Male patient, 39 years old, complaning about vomiting, hyperpigmented skin associated with abolish, psicoses, urinary incontinence, temporal and spacial confusion as well as were found: hyperkalaemia, hyponatremia, hypoglycemia, elevated ACTH levels, basal cortisol decresead, antibody anti-21-hidroxilase non reagente, screening for infectious agents were carried out and infection subsequently ruled out. Were observed in MRI Brain: hypersignal in cerebral white matter on T2-FLAIR sequence bilaterally in which the occipitoparietal region, frontal lobe and basal ganglia were more affected. After metabolic and hydroelectric disorders estabilization using Prednisone, Fludrocortisone per day for 5 days, he evolved with worsening of cognitive and behavioral status until nowdays. Actually, he is totally dependent on his basic activities. Conclusions: It is a rare disease, but it must be recognized by every neurologist, since it is can affect other systems and can leave serious sequelae.

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FACON, T., J. GOUPEMAND, C. CARON, M. ZANDECKI, M. H. ESTIENNE, and A. COSSON. "GRAY PLATELET SYNDROME AND IDIOPATHIC PULMONARY FIBROSIS OCCURRING IN THE SAME PATIENT : A FORTUITOUS ASSOCIATION?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644559.

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A 46 yr old Caucasian woman has been diagnosed as having a congenital deficiency of platelet a-granules (gray platelet syndrome - GPS) associated with an extensive idiopathic pulmonary fibrosis (IPF). The patient had a life long history of bleeding tendency including dental bleedings in childhood, intraperitoneal bleeding, metrorrhagias which led to hysterectomy, and post-operative hemorrhages. When aged 16, splenectomy was performed because of a mild thrombocytopenia but did not result in a subsequent improvement of the platelet count. The spleen was enlarged and showed an excess of fibrous tissue.Evaluation of hemostasis (July 1986) revealed a moderate thrombocytopenia of 120 × 109/1 constrasting with a markedly prolonged Simplate bleeding time (>30 min.). When examined on stained blood films, the platelets presented a "ghost-like" gray appearance. The mean platelet volume (coulter S + IV) was increased to 14 μ3 (N : 6.5-9.5 μ3). Ultrastructural studies confirmed the lack of a-granules and showed normal presence of dense-bodies, mitochondria and peroxisomes. Platelet aggregation was decreased when induced by thrombin, ADP and collagen but normal in response to arachidonic acid and ristocetin. A severely decreased content of platelet proteins such as fibrinogen, vWF:Ag, BTG and PF4. was further demonstrated. A bone marrow biopsy performed on March 1986 gave no evidence of myelofibrosis (occasionally recorded in GPS) but the patient developed for these last 6 years a severe IPF requiring a permanent oxygen-therapy. Although the association GPS-IPF might be only considered as a fortuitous one, we hypothesize that these two events might be related to each other, possibly through the presence of megakaryocytes in pulmonary capillaries, in the same way as bone marrow fibrosis has been suggested as a possible consequence of the lack of a-granules in GPS (DR0UET et al. - Nouv. Rev. Fr. Hematol., 1981, 23 : 95).

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Hawkins, J., and M. Boden. "Predicting Peroxisomal Proteins." In 2005 IEEE Symposium on Computational Intelligence in Bioinformatics and Computational Biology. IEEE, 2005. http://dx.doi.org/10.1109/cibcb.2005.1594956.

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"Targeting peroxisomal transport in trypanosoma." In 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.566.

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Human infection with Trypanosoma parasites (Chagas disease and Human African Trypanosomiasis) affects around 10 million people worldwide resulting in life-threatening disease. Treatment options are limited to historic drugs characterized by significant side effects and decreasing efficacy while new drug development efforts are largely neglected. Here, we review drug discovery effort in human trypanosomiasis undertaken in academia. Peroxisomal (Pex) transport system was validated as a target in Chagas disease and a number of compounds were delivered which have shown promising results in animal experiments. Future perspectives of exploring the Pex system in anti-trypanosoma drug development are discussed.

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Smith, Steven G., Roma Sehmi, Karen Howie, Richard M. Watson, Heather Campbell, George Obminski, and Gail M. Gauvreau. "Effects Of Peroxisome Proliferator-Activated Receptors (PPARs) On Eosinophil Migration." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2787.

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Reports on the topic "Peroxisomes"

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Friedman, Haya, Chris Watkins, Susan Lurie, and Susheng Gan. Dark-induced Reactive Oxygen Species Accumulation and Inhibition by Gibberellins: Towards Inhibition of Postharvest Senescence. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7613883.bard.

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Dark-induced senescence could pose a major problem in export of various crops including cuttings. The assumption of this work was that ROS which is increased at a specific organelle can serve as a signal for activation of cell senescence program. Hormones which reduce senescence in several crops like gibberellic acid (GA) and possibly cytokinin (CK) may reduce senescence by inhibiting this signal. In this study we worked on Pelargonium cuttings as well as Arabidopsis rosette. In Pelargonium the increase in ROS occurred concomitantly with increase in two SAGs, and the increase persisted in isolated chloroplasts. In Arabidopsis we used two recentlydeveloped technologies to examine these hypotheses; one is a transcriptome approach which, on one hand, enabled to monitor expression of genes within the antioxidants network, and on the other hand, determine organelle-specific ROS-related transcriptome footprint. This last approach was further developed to an assay (so called ROSmeter) for determination of the ROS-footprint resulting from defined ROS stresses. The second approach involved the monitoring of changes in the redox poise in different organelles by measuring fluorescence ratio of redox-sensitive GFP (roGFP) directed to plastids, mitochondria, peroxisome and cytoplasm. By using the roGFP we determined that the mitochondria environment is oxidized as early as the first day under darkness, and this is followed by oxidation of the peroxisome on the second day and the cytoplast on the third day. The plastids became less oxidized at the first day of darkness and this was followed by a gradual increase in oxidation. The results with the ROS-related transcriptome footprint showed early changes in ROS-related transcriptome footprint emanating from mitochondria and peroxisomes. Taken together these results suggest that the first ROS-related change occurred in mitochondria and peroxisomes. The analysis of antioxidative gene’s network did not yield any clear results about the changes occurring in antioxidative status during extended darkness. Nevertheless, there is a reduction in expression of many of the plastids antioxidative related genes. This may explain a later increase in the oxidation poise of the plastids, occurring concomitantly with increase in cell death. Gibberellic acid (GA) prevented senescence in Pelargonium leaves; however, in Arabidopsis it did not prevent chlorophyll degradation, but prevented upregulation of SAGs (Apendix Fig. 1). Gibberellic acid prevented in Pelargonium the increase in ROS in chloroplast, and we suggested that this prevents the destruction of the chloroplasts and hence, the tissue remains green. In Arabidopsis, reduction in endogenous GA and BA are probably not causing dark-induced senescence, nevertheless, these materials have some effect at preventing senescence. Neither GA nor CK had any effect on transcriptome footprint related to ROS in the various organelles, however while GA reduced expression of few general ROS-related genes, BA mainly prevented the decrease in chloroplasts genes. Taken together, GA and BA act by different pathways to inhibit senescence and GA might act via ROS reduction. Therefore, application of both hormones may act synergistically to prevent darkinduced senescence of various crops.

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DeLoache, William, Zachary Russ, Jennifer Samson, and John Dueber. Repurposing the Saccharomyces cerevisiae peroxisome for compartmentalizing multi-enzyme pathways. Office of Scientific and Technical Information (OSTI), September 2017. http://dx.doi.org/10.2172/1394729.

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Tarr, Melinda J., and Larry E. Mathes. Investigation of the Hepatotoxic and Immunotoxic Effects of the Peroxisome Proliferator Perfluorodecanoic Acid. Fort Belvoir, VA: Defense Technical Information Center, April 1992. http://dx.doi.org/10.21236/ada250176.

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Frazier, Donald E., and Melinda J. Tarr. Investigation of the Hepatotoxic and Immunotoxic Effects of the Peroxisome Proliferator Perfluorodecanoic Acid. Fort Belvoir, VA: Defense Technical Information Center, April 1991. http://dx.doi.org/10.21236/ada237787.

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Allred, Clinton D. Defining the Molecular Actions of Dietary Fatty Acids in Breast Cancer: Selective Modulation of Peroxisome Proliferator-Activated Receptor Gamma. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada437097.

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Allred, Clinton D., and Michael W. Kilgore. Defining the Molecular Actions of Dietary Fatty Acids in Breast Cancer: Selective Modulation of Peroxisome Proliferator-Activated Receptor Gamma. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada463408.

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Allred, Clinton D., and Michael W. Kilgore. Defining the Molecular Actions of Dietary Fatty Acids in Breast Cancer: Selective Modulation of Peroxisome Proliferator-Activated Receptor Gamma. Addendum. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada484949.

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Katzenellenbogen, John, A. Novel Chemical Strategies for Labeling Small Molecule Ligands for Androgen, Progestin, and Peroxisome Proliferator-Activated Receptors for Imaging Prostate and Breast Cancer and the Heart. Office of Scientific and Technical Information (OSTI), April 2007. http://dx.doi.org/10.2172/902426.

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Droby, Samir, Michael Wisniewski, Ron Porat, and Dumitru Macarisin. Role of Reactive Oxygen Species (ROS) in Tritrophic Interactions in Postharvest Biocontrol Systems. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7594390.bard.

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To elucidate the role of ROS in the tri-trophic interactions in postharvest biocontrol systems a detailed molecular and biochemical investigation was undertaken. The application of the yeast biocontrol agent Metschnikowia fructicola, microarray analysis was performed on grapefruit surface wounds using an Affymetrix Citrus GeneChip. the data indicated that 1007 putative unigenes showed significant expression changes following wounding and yeast application relative to wounded controls. The expression of the genes encoding Respiratory burst oxidase (Rbo), mitogen-activated protein kinase (MAPK) and mitogen-activated protein kinase kinase (MAPKK), G-proteins, chitinase (CHI), phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS) and 4-coumarate-CoA ligase (4CL). In contrast, three genes, peroxidase (POD), superoxide dismutase (SOD) and catalase (CAT), were down-regulated in grapefruit peel tissue treated with yeast cells. The yeast antagonists, Metschnikowia fructicola (strain 277) and Candida oleophila (strain 182) generate relatively high levels of super oxide anion (O2−) following its interaction with wounded fruit surface. Using laser scanning confocal microscopy we observed that the application of M. fructicola and C. oleophila into citrus and apple fruit wounds correlated with an increase in H2O2 accumulation in host tissue. The present data, together with our earlier discovery of the importance of H₂O₂ production in the defense response of citrus flavedo to postharvest pathogens, indicate that the yeast-induced oxidative response in fruit exocarp may be associated with the ability of specific yeast species to serve as biocontrol agents for the management of postharvest diseases. Effect of ROS on yeast cells was also studied. Pretreatment of the yeast, Candida oleophila, with 5 mM H₂O₂ for 30 min (sublethal) increased yeast tolerance to subsequent lethal levels of oxidative stress (50 mM H₂O₂), high temperature (40 °C), and low pH (pH 4). Suppression subtractive hybridization analysis was used to identify genes expressed in yeast in response to sublethal oxidative stress. Transcript levels were confirmed using semi quantitative reverse transcription-PCR. Seven antioxidant genes were up regulated. Pretreatment of the yeast antagonist Candida oleophila with glycine betaine (GB) increases oxidative stress tolerance in the microenvironment of apple wounds. ROS production is greater when yeast antagonists used as biocontrol agents are applied in the wounds. Compared to untreated control yeast cells, GB-treated cells recovered from the oxidative stress environment of apple wounds exhibited less accumulation of ROS and lower levels of oxidative damage to cellular proteins and lipids. Additionally, GB-treated yeast exhibited greater biocontrol activity against Penicillium expansum and Botrytis cinerea, and faster growth in wounds of apple fruits compared to untreated yeast. The expression of major antioxidant genes, including peroxisomal catalase, peroxiredoxin TSA1, and glutathione peroxidase was elevated in the yeast by GB treatment. A mild heat shock (HS) pretreatment (30 min at 40 1C) improved the tolerance of M. fructicola to subsequent high temperature (45 1C, 20–30 min) and oxidative stress (0.4 mol-¹) hydrogen peroxide, 20–60 min). HS-treated yeast cells showed less accumulation of reactive oxygen species (ROS) than non-treated cells in response to both stresses. Additionally, HS-treated yeast exhibited significantly greater (P≥0.0001) biocontrol activity against Penicillium expansum and a significantly faster (Po0.0001) growth rate in wounds of apple fruits stored at 25 1C compared with the performance of untreated yeast cells. Transcription of a trehalose-6-phosphate synthase gene (TPS1) was up regulated in response to HS and trehalose content also increased.

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Fluhr, Robert, and Maor Bar-Peled. Novel Lectin Controls Wound-responses in Arabidopsis. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697123.bard.

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Innate immune responses in animals and plants involve receptors that recognize microbe-associated molecules. In plants, one set of this defense system is characterized by large families of TIR–nucleotide binding site–leucine-rich repeat (TIR-NBS-LRR) resistance genes. The direct interaction between plant proteins harboring the TIR domain with proteins that transmit and facilitate a signaling pathway has yet to be shown. The Arabidopsis genome encodes TIR-domain containing genes that lack NBS and LRR whose functions are unknown. Here we investigated the functional role of such protein, TLW1 (TIR LECTIN WOUNDRESPONSIVE1). The TLW1 gene encodes a protein with two domains: a TIR domain linked to a lectin-containing domain. Our specific aim in this proposal was to examine the ramifications of the TL1-glycan interaction by; A) The functional characterization of TL1 activity in the context of plant wound response and B) Examine the hypothesis that wounding induced specific polysaccharides and examine them as candidates for TL-1 interactive glycan compounds. The Weizmann group showed TLW1 transcripts are rapidly induced by wounding in a JA-independent pathway and T-DNA-tagged tlw1 mutants that lack TLW1 transcripts, fail to initiate the full systemic wound response. Transcriptome methodology analysis was set up and transcriptome analyses indicates a two-fold reduced level of JA-responsive but not JA-independent transcripts. The TIR domain of TLW1 was found to interact directly with the KAT2/PED1 gene product responsible for the final b-oxidation steps in peroxisomal-basedJA biosynthesis. To identify potential binding target(s) of TL1 in plant wound response, the CCRC group first expressed recombinant TL1 in bacterial cells and optimized conditions for the protein expression. TL1 was most highly expressed in ArcticExpress cell line. Different types of extraction buffers and extraction methods were used to prepare plant extracts for TL1 binding assay. Optimized condition for glycan labeling was determined, and 2-aminobenzamide was used to label plant extracts. Sensitivity of MALDI and LC-MS using standard glycans. THAP (2,4,6- Trihydroxyacetophenone) showed minimal background peaks at positive mode of MALDI, however, it was insensitive with a minimum detection level of 100 ng. Using LC-MS, sensitivity was highly increased enough to detect 30 pmol concentration. However, patterns of total glycans displayed no significant difference between different extraction conditions when samples were separated with Dionex ICS-2000 ion chromatography system. Transgenic plants over-expressing lectin domains were generated to obtain active lectin domain in plant cells. Insertion of the overexpression construct into the plant genome was confirmed by antibiotic selection and genomic DNA PCR. However, RT-PCR analysis was not able to detect increased level of the transcripts. Binding ability of azelaic acid to recombinant TL1. Azelaic acid was detected in GST-TL1 elution fraction, however, DHB matrix has the same mass in background signals, which needs to be further tested on other matrices. The major findings showed the importance of TLW1 in regulating wound response. The findings demonstrate completely novel and unexpected TIR domain interactions and reveal a control nexus and mechanism that contributes to the propagation of wound responses in Arabidopsis. The implications are to our understanding of the function of TIR domains and to the notion that early molecular events occur systemically within minutes of a plant sustaining a wound. A WEB site (http://genome.weizmann.ac.il/hormonometer/) was set up that enables scientists to interact with a collated plant hormone database.

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