Relevant bibliographies by topics / Plant autophagy

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Plant autophagy'

Author: Grafiati
Published: 28 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Plant autophagy"

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Luo, Shuwei, Xifeng Li, Yan Zhang, Yunting Fu, Baofang Fan, Cheng Zhu, and Zhixiang Chen. "Cargo Recognition and Function of Selective Autophagy Receptors in Plants." International Journal of Molecular Sciences 22, no. 3 (January 20, 2021): 1013. http://dx.doi.org/10.3390/ijms22031013.

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Autophagy is a major quality control system for degradation of unwanted or damaged cytoplasmic components to promote cellular homeostasis. Although non-selective bulk degradation of cytoplasm by autophagy plays a role during cellular response to nutrient deprivation, the broad roles of autophagy are primarily mediated by selective clearance of specifically targeted components. Selective autophagy relies on cargo receptors that recognize targeted components and recruit them to autophagosomes through interaction with lapidated autophagy-related protein 8 (ATG8) family proteins anchored in the membrane of the forming autophagosomes. In mammals and yeast, a large collection of selective autophagy receptors have been identified that mediate the selective autophagic degradation of organelles, aggregation-prone misfolded proteins and other unwanted or nonnative proteins. A substantial number of selective autophagy receptors have also been identified and functionally characterized in plants. Some of the autophagy receptors in plants are evolutionarily conserved with homologs in other types of organisms, while a majority of them are plant-specific or plant species-specific. Plant selective autophagy receptors mediate autophagic degradation of not only misfolded, nonactive and otherwise unwanted cellular components but also regulatory and signaling factors and play critical roles in plant responses to a broad spectrum of biotic and abiotic stresses. In this review, we summarize the research on selective autophagy in plants, with an emphasis on the cargo recognition and the biological functions of plant selective autophagy receptors.
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Zeng, Yonglun, Baiying Li, Changyang Ji, Lei Feng, Fangfang Niu, Cesi Deng, Shuai Chen, et al. "A unique AtSar1D-AtRabD2a nexus modulates autophagosome biogenesis in Arabidopsis thaliana." Proceedings of the National Academy of Sciences 118, no. 17 (April 20, 2021): e2021293118. http://dx.doi.org/10.1073/pnas.2021293118.

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In eukaryotes, secretory proteins traffic from the endoplasmic reticulum (ER) to the Golgi apparatus via coat protein complex II (COPII) vesicles. Intriguingly, during nutrient starvation, the COPII machinery acts constructively as a membrane source for autophagosomes during autophagy to maintain cellular homeostasis by recycling intermediate metabolites. In higher plants, essential roles of autophagy have been implicated in plant development and stress responses. Nonetheless, the membrane sources of autophagosomes, especially the participation of the COPII machinery in the autophagic pathway and autophagosome biogenesis, remains elusive in plants. Here, we provided evidence in support of a novel role of a specific Sar1 homolog AtSar1d in plant autophagy in concert with a unique Rab1/Ypt1 homolog AtRabD2a. First, proteomic analysis of the plant ATG (autophagy-related gene) interactome uncovered the mechanistic connections between ATG machinery and specific COPII components including AtSar1d and Sec23s, while a dominant negative mutant of AtSar1d exhibited distinct inhibition on YFP-ATG8 vacuolar degradation upon autophagic induction. Second, a transfer DNA insertion mutant of AtSar1d displayed starvation-related phenotypes. Third, AtSar1d regulated autophagosome progression through specific recognition of ATG8e by a noncanonical motif. Fourth, we demonstrated that a plant-unique Rab1/Ypt1 homolog AtRabD2a coordinates with AtSar1d to function as the molecular switch in mediating the COPII functions in the autophagy pathway. AtRabD2a appears to be essential for bridging the specific AtSar1d-positive COPII vesicles to the autophagy initiation complex and therefore contributes to autophagosome formation in plants. Taken together, we identified a plant-specific nexus of AtSar1d-AtRabD2a in regulating autophagosome biogenesis.
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Gao, Caiji, Xiaohong Zhuang, Yong Cui, Xi Fu, Yilin He, Qiong Zhao, Yonglun Zeng, Jinbo Shen, Ming Luo, and Liwen Jiang. "Dual roles of an Arabidopsis ESCRT component FREE1 in regulating vacuolar protein transport and autophagic degradation." Proceedings of the National Academy of Sciences 112, no. 6 (January 26, 2015): 1886–91. http://dx.doi.org/10.1073/pnas.1421271112.

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Protein turnover can be achieved via the lysosome/vacuole and the autophagic degradation pathways. Evidence has accumulated revealing that efficient autophagic degradation requires functional endosomal sorting complex required for transport (ESCRT) machinery. However, the interplay between the ESCRT machinery and the autophagy regulator remains unclear. Here, we show that FYVE domain protein required for endosomal sorting 1 (FREE1), a recently identified plant-specific ESCRT component essential for multivesicular body (MVB) biogenesis and plant growth, plays roles both in vacuolar protein transport and autophagic degradation. FREE1 also regulates vacuole biogenesis in both seeds and vegetative cells of Arabidopsis. Additionally, FREE1 interacts directly with a unique plant autophagy regulator SH3 DOMAIN-CONTAINING PROTEIN2 and associates with the PI3K complex, to regulate the autophagic degradation in plants. Thus, FREE1 plays multiple functional roles in vacuolar protein trafficking and organelle biogenesis as well as in autophagic degradation via a previously unidentified regulatory mechanism of cross-talk between the ESCRT machinery and autophagy process.
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Yang, Meng, Asigul Ismayil, and Yule Liu. "Autophagy in Plant-Virus Interactions." Annual Review of Virology 7, no. 1 (September 29, 2020): 403–19. http://dx.doi.org/10.1146/annurev-virology-010220-054709.

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Autophagy is a conserved vacuole/lysosome-mediated degradation pathway for clearing and recycling cellular components including cytosol, macromolecules, and dysfunctional organelles. In recent years, autophagy has emerged to play important roles in plant-pathogen interactions. It acts as an antiviral defense mechanism in plants. Moreover, increasing evidence shows that plant viruses can manipulate, hijack, or even exploit the autophagy pathway to promote pathogenesis, demonstrating the pivotal role of autophagy in the evolutionary arms race between hosts and viruses. In this review, we discuss recent findings about the antiviral and proviral roles of autophagy in plant-virus interactions.
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Zhang, Tianrui, Zhidan Xiao, Chuanliang Liu, Chao Yang, Jiayi Li, Hongbo Li, Caiji Gao, and Wenjin Shen. "Autophagy Mediates the Degradation of Plant ESCRT Component FREE1 in Response to Iron Deficiency." International Journal of Molecular Sciences 22, no. 16 (August 16, 2021): 8779. http://dx.doi.org/10.3390/ijms22168779.

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Multivesicular body (MVB)-mediated endosomal sorting and macroautophagy are the main pathways mediating the transport of cellular components to the vacuole and are essential for maintaining cellular homeostasis. The interplay of these two pathways remains poorly understood in plants. In this study, we show that FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING 1 (FREE1), which was previously identified as a plant-specific component of the endosomal sorting complex required for transport (ESCRT), essential for MVB biogenesis and plant growth, can be transported to the vacuole for degradation in response to iron deficiency. The vacuolar transport of ubiquitinated FREE1 protein is mediated by the autophagy pathway. As a consequence, the autophagy deficient mutants, atg5-1 and atg7-2, accumulate more endogenous FREE1 protein and display hypersensitivity to iron deficiency. Furthermore, under iron-deficient growth condition autophagy related genes are upregulated to promote the autophagic degradation of FREE1, thereby possibly relieving the repressive effect of FREE1 on iron absorption. Collectively, our findings demonstrate a unique regulatory mode of protein turnover of the ESCRT machinery through the autophagy pathway to respond to iron deficiency in plants.
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Ran, Jie, Sayed M. Hashimi, and Jian-Zhong Liu. "Emerging Roles of the Selective Autophagy in Plant Immunity and Stress Tolerance." International Journal of Molecular Sciences 21, no. 17 (August 31, 2020): 6321. http://dx.doi.org/10.3390/ijms21176321.

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Autophagy is a conserved recycling system required for cellular homeostasis. Identifications of diverse selective receptors/adaptors that recruit appropriate autophagic cargoes have revealed critical roles of selective autophagy in different biological processes in plants. In this review, we summarize the emerging roles of selective autophagy in both biotic and abiotic stress tolerance and highlight the new features of selective receptors/adaptors and their interactions with both the cargoes and Autophagy-related gene 8s (ATG8s). In addition, we review how the two major degradation systems, namely the ubiquitin–proteasome system (UPS) and selective autophagy, are coordinated to cope with stress in plants. We especially emphasize how plants develop the selective autophagy as a weapon to fight against pathogens and how adapted pathogens have evolved the strategies to counter and/or subvert the immunity mediated by selective autophagy.
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Hafrén, Anders, Jean-Luc Macia, Andrew J. Love, Joel J. Milner, Martin Drucker, and Daniel Hofius. "Selective autophagy limits cauliflower mosaic virus infection by NBR1-mediated targeting of viral capsid protein and particles." Proceedings of the National Academy of Sciences 114, no. 10 (February 21, 2017): E2026—E2035. http://dx.doi.org/10.1073/pnas.1610687114.

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Autophagy plays a paramount role in mammalian antiviral immunity including direct targeting of viruses and their individual components, and many viruses have evolved measures to antagonize or even exploit autophagy mechanisms for the benefit of infection. In plants, however, the functions of autophagy in host immunity and viral pathogenesis are poorly understood. In this study, we have identified both anti- and proviral roles of autophagy in the compatible interaction of cauliflower mosaic virus (CaMV), a double-stranded DNA pararetrovirus, with the model plantArabidopsis thaliana. We show that the autophagy cargo receptor NEIGHBOR OF BRCA1 (NBR1) targets nonassembled and virus particle-forming capsid proteins to mediate their autophagy-dependent degradation, thereby restricting the establishment of CaMV infection. Intriguingly, the CaMV-induced virus factory inclusions seem to protect against autophagic destruction by sequestering capsid proteins and coordinating particle assembly and storage. In addition, we found that virus-triggered autophagy prevents extensive senescence and tissue death of infected plants in a largely NBR1-independent manner. This survival function significantly extends the timespan of virus production, thereby increasing the chances for virus particle acquisition by aphid vectors and CaMV transmission. Together, our results provide evidence for the integration of selective autophagy into plant immunity against viruses and reveal potential viral strategies to evade and adapt autophagic processes for successful pathogenesis.
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Acheampong, Atiako Kwame, Carly Shanks, Chia-Yi Cheng, G. Eric Schaller, Yasin Dagdas, and Joseph J. Kieber. "EXO70D isoforms mediate selective autophagic degradation of type-A ARR proteins to regulate cytokinin sensitivity." Proceedings of the National Academy of Sciences 117, no. 43 (October 13, 2020): 27034–43. http://dx.doi.org/10.1073/pnas.2013161117.

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The phytohormone cytokinin influences many aspects of plant growth and development, several of which also involve the cellular process of autophagy, including leaf senescence, nutrient remobilization, and developmental transitions. The Arabidopsis type-A response regulators (type-A ARR) are negative regulators of cytokinin signaling that are transcriptionally induced in response to cytokinin. Here, we describe a mechanistic link between cytokinin signaling and autophagy, demonstrating that plants modulate cytokinin sensitivity through autophagic regulation of type-A ARR proteins. Type-A ARR proteins were degraded by autophagy in an AUTOPHAGY-RELATED (ATG)5-dependent manner, and this degradation is promoted by phosphorylation on a conserved aspartate in the receiver domain of the type-A ARRs. EXO70D family members interacted with type-A ARR proteins, likely in a phosphorylation-dependent manner, and recruited them to autophagosomes via interaction of the EXO70D AIM with the core autophagy protein, ATG8. Consistently, loss-of-function exo70D1,2,3 mutants exhibited compromised targeting of type-A ARRs to autophagic vesicles, have elevated levels of type-A ARR proteins, and are hyposensitive to cytokinin. Disruption of both type-A ARRs and EXO70D1,2,3 compromised survival in carbon-deficient conditions, suggesting interaction between autophagy and cytokinin responsiveness in response to stress. These results indicate that the EXO70D proteins act as selective autophagy receptors to target type-A ARR cargos for autophagic degradation, demonstrating modulation of cytokinin signaling by selective autophagy.
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Bao, Yan, Wei-Meng Song, Peipei Wang, Xiang Yu, Bei Li, Chunmei Jiang, Shin-Han Shiu, Hongxia Zhang, and Diane C. Bassham. "COST1 regulates autophagy to control plant drought tolerance." Proceedings of the National Academy of Sciences 117, no. 13 (March 13, 2020): 7482–93. http://dx.doi.org/10.1073/pnas.1918539117.

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Plants balance their competing requirements for growth and stress tolerance via a sophisticated regulatory circuitry that controls responses to the external environments. We have identified a plant-specific gene, COST1 (constitutively stressed 1), that is required for normal plant growth but negatively regulates drought resistance by influencing the autophagy pathway. An Arabidopsis thaliana cost1 mutant has decreased growth and increased drought tolerance, together with constitutive autophagy and increased expression of drought-response genes, while overexpression of COST1 confers drought hypersensitivity and reduced autophagy. The COST1 protein is degraded upon plant dehydration, and this degradation is reduced upon treatment with inhibitors of the 26S proteasome or autophagy pathways. The drought resistance of a cost1 mutant is dependent on an active autophagy pathway, but independent of other known drought signaling pathways, indicating that COST1 acts through regulation of autophagy. In addition, COST1 colocalizes to autophagosomes with the autophagosome marker ATG8e and the autophagy adaptor NBR1, and affects the level of ATG8e protein through physical interaction with ATG8e, indicating a pivotal role in direct regulation of autophagy. We propose a model in which COST1 represses autophagy under optimal conditions, thus allowing plant growth. Under drought, COST1 is degraded, enabling activation of autophagy and suppression of growth to enhance drought tolerance. Our research places COST1 as an important regulator controlling the balance between growth and stress responses via the direct regulation of autophagy.
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Zenkov, N. K., A. V. Chechushkov, P. M. Kozhin, N. V. Kandalintseva, G. G. Martinovich, and E. B. Menshchikova. "Plant phenols and autophagy." Biochemistry (Moscow) 81, no. 4 (April 2016): 297–314. http://dx.doi.org/10.1134/s0006297916040015.

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Dissertations / Theses on the topic "Plant autophagy"

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Ballhaus, Florentine. "Investigating plant autophagy with new chemical modulators." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-428075.

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Autophagy is a major catabolic pathway in which cell components get sequestered in a double membrane vesicle, transported to the vacuole, degraded by vacuolar hydrolases and recycled.  Through this process, cells ensure cell homeostasis and remobilise nutrients. The autophagic flux can be enhanced as an adaptive stress response, improving plants resistance against stress, reducing aging and ultimately increasing yield. However, autophagy regulation in plants remains poorly understood.  Novel plant-specific modulators can be used in a chemical genetic approach for identification of proteins involved in the autophagy pathway. Furthermore, autophagy enhancers can find their application in agriculture for improved plant fitness. Known autophagy modulators have severe off-target effects, affecting plant growth and development. A recent screening identified two potential autophagy modulators. We developed a novel method for photoaffinity labelling and pulldown assay in Arabidopsis thaliana to identify potential interactors of the modulators. The identification of autophagy-related proteins will help to further elucidate the autophagic pathway in plants. The effect of the new autophagy enhancers on plant growth and development was analysed by automated growth assays. In comparison with a currently available autophagy enhancer, treated plants showed higher viability, indicating possible further applications for the new autophagy modulators in planta.
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Gomez, Rodrigo Enrique. "Unravelling the contribution of lipids in plant autophagy : Identification and functional characterization of lipids implicated in the autophagic process in Arabidopsis." Thesis, Bordeaux, 2021. http://www.theses.fr/2021BORD0103.

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Les plantes, étant des organismes sessiles, sont fréquemment confrontées à une grande variété de stress environnementaux. Ces conditions peuvent conduire à l'accumulation d'agrégats de protéines ou au disfonctionnement de multiples organites intracellulaires. Pour faire face à ces conditions, les plantes ont mis au point des mécanismes d'adaptation sophistiqués qui permettent le recyclage des composants intracellulaires. Ces mécanismes sont essentiels pour les remodelages métaboliques nécessaires à un recyclage efficace des nutriments ainsi qu'à l'élimination des composants nocifs pour la cellule comme des organites endommagés. L'un de ces mécanismes est l'autophagie, une voie de dégradation intracellulaire qui utilise des vésicules à double membrane qui encapsulent des portions du cytoplasme et le délivrent à la vacuole où elles sont dégradées. L'autophagie repose sur la formation de ces vésicules spécialisées, appelées autophagosomes (AP). Les AP sont des vésicules uniques dans le système endomembranaire, d'abord parce qu'elles sont constituées d'une double couche lipidique, et ensuite parce qu'elles ne bourgeonnent pas à partir d'un compartiment déjà existant. La biogenèse des AP est un processus en plusieurs étapes impliquant une machinerie centrale (protéines ATG) qui intervient dans la formation de novo d'une membrane initiale ; puis, par l'addition de lipides, cette membrane s’agrandit et devient une structure en forme de coupe avec des bords fortement incurvés lui permettant d’engloutir la cargaison autophagique. Une fois la cargaison engloutie, ses bords fusionnent afin de fermer la structure, qui circule ensuite vers la vacuole, où sa membrane externe fusionne avec la membrane de la vacuole ce qui libère la membrane interne et la cargaison à l'intérieur de la vacuole pour sa dégradation. Ainsi, la biogenèse des AP repose sur de nombreux événements de remodelage membranaire, d'abord pour initier la membrane initiale, puis pour maintenir sa forme très incurvée tout en assurant son expansion, et enfin pour sceller les structures matures et promouvoir sa fusion ultérieure à la vacuole. Dans les membranes biologiques, les lipides, grâce à leurs propriétés physico-chimiques, définissent des caractéristiques importantes telles que la fluidité, la courbure ainsi que les champs électrostatiques des membranes. Par conséquent, le rôle crucial des lipides dans l'autophagie a émergé ces dernières années. Chez les plantes, on ne connait encore que très peu de choses sur la composition lipidique des membranes autophagiques et les fonctions des lipides dans la formation des AP restent largement méconnu. Mon travail de thèse a consisté à identifier des acteurs lipidiques et protéiques impliquées dans l'autophagie chez les plantes dans le but de caractériser leur fonction dans le processus. En effectuant un criblage d'inhibiteurs enzymatiques nous avons analysé l'impact de l'inhibition de la synthèse de différentes espèces de lipides sur l'autophagie. En utilisant cette approche, nous avons identifié différents candidats lipidiques importants pour l'autophagie des plantes. Notamment, nous avons identifié le phosphatydilinositol-4-phosphate (PI4P) comme étant critique pour la formation des APs. En l'absence dePI4P, la formation des AP est stoppée à un stade très précoce, ce qui entraîne un blocage total dans le processus. De plus, nous avons obtenu des informations précieuses pour mieux comprendre la formation des APs chez les plantes. En particulier, nos résultats suggèrent que la membrane plasmique (PM) semble jouer un rôle important dans la formation de ces structures. Dans leur ensemble, nos résultats ont confirmé notre hypothèse initiale: les lipides ne sont pas seulement des éléments inertes qui constituent les membranes autophagiques ;ils semblent plutôt jouer des rôles distincts et avoir des fonctions spécifiques dans le processus
Plants, being sessile organisms, are frequently confronted to a plethora of environmental stresses and harsh conditions. Enduring these conditions can lead to the accumulation of protein aggregates or organelles that become dysfunctional. To withstand these conditions, plants have evolved sophisticated adaptation mechanisms for the recycling of intracellular components. These mechanisms are essential for the metabolic transitions required for efficient nutrient use, as well as proper disposal of protein aggregates or damaged organelles. One of these mechanisms is autophagy, an intracellular degradation pathway that employs specialized double membrane vesicles that encapsulate cytosolic material and delivers it to the vacuole for degradation. Autophagy relies on the formation of these specialized vesicles, called autophagosomes (APs). APs are unique vesicles in the endomembrane system, first because they are made of a double lipid bilayer, and second because they do not but from a pre-existing compartment. AP biogenesis is a multistep process implicating a core machinery (ATG proteins) that mediate the de novo formation of an initial membrane; then, by the addition of lipids, this membrane expands into a cup-shaped structure with highly curved edges to engulf autophagic cargo. Upon completion, the rims of the structure seal and form a mature AP that traffics to the vacuole, where its outer membrane fuses with the tonoplast releasingthe inner membrane and cargo inside the vacuole. Thus, AP biogenesis relies on numerous membrane remodeling events, first to initiate the initial membrane, then to maintain the highly curved shape of the structure while ensuring its expansion, and finally to seal the mature structures and its subsequent fusion to the vacuole. Lipids, thanks to their physicochemical properties define important membrane features such as its, fluidity, curvature and electrostatics. Hence, evidence showing the crucial role of lipids in autophagy has emerged in the recent years. In plants however, little is known about the lipid composition of autophagic membranes and thus, about the functional contribution of lipids in plant autophagy. My PhD thesis consisted on identifying crucial lipids for plant autophagy with an aim to characterize their function in the process. By performing a lipid-related enzymes inhibitor screen in which we assayed the impact of inhibiting the synthesis of specific lipids on autophagy, we identified different lipid candidates important for plant autophagy. Notably, we identified the phosphatydil-inositol-4-phosphate (PI4P) as being critical for the formation of APs. In the absence of PI4P, AP formation is stalled at a very early stage resulting in a block in the process. Furthermore, we have obtained valuable insights to better understand the AP formation. In plants, particularly, our results suggest that the plasma membrane (PM) plays important roles in the formation of these structures. Taken together, our results confirmed that lipids are more than just building blocks constituting the autophagic membranes; rather, they seem to play distinct and specific roles in the pathway. Finally, this thesis highlights how lipids are key actors for the autophagic process and thus for plants adaptations to adverse and stressful environmental conditions
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Testi, Serena. "L’effecteur Avh195 de Phytophthora parasitica : antagoniste de l’autophagie chez l’hôte et promoteur du processus infectieux." Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4087/document.

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L’agent pathogène Phytophthora parasitica est un oomycète qui a des effets dévastateurs sur l’agriculture et les écosystèmes naturels. En tant qu'organisme hémi-biotrophe, il infecte les racines des plantes en établissant d'abord un contact intime avec les cellules hôtes (biotrophie) avant de les tuer (nécrotrophie) et de terminer son cycle d'infection. Pour contrôler ces processus, les oomycètes sécrètent des protéines effectrices, qui sont internalisées dans les cellules végétales par un motif de translocation (appelé RxLR-EER) pour manipuler la physiologie et les réponses immunitaires de l'hôte. Les études des échanges moléculaires entre Phytophthora parasitica et la plante qui ont été menées par le laboratoire d'accueil ont permis d'identifier un effecteur RxLR, dénommé Avh195. La séquence en acides aminés de l'effecteur est caractérisée par la présence de cinq motifs AIM (« ATG8 Interacting Motive ») qui indiquent une interaction potentielle avec la protéine centrale de l’autophagie, ATG8. Avh195 co-localise avec la fraction membranaire de l'ATG8, et un système double-hybride en levure permettant la détermination d’interactions entre protéines membranaires, a confirmé une interaction non sélective entre Avh195 et plusieurs isoformes d'ATG8. La caractérisation de la perturbation de l'autophagie dépendante de Avh195 a été réalisée dans l'algue unicellulaire Chlamydomonas reinhardtii après génération de lignées transgéniques surexprimant l'effecteur. Les analyses par cytométrie de flux ont révélé que Avh195 ne modifie pas la physiologie et la « fitness » de l'algue dans des conditions de croissance normales et pendant l'autophagie induite par la rapamycine. La microscopie électronique à transmission a révélé que l'effecteur provoque dans les cellules de l’algue un retard dans le flux autophagique, se traduisant par une réduction de la coalescence et de la clairance des vacuoles et une forte accumulation d'amidon dans les chloroplastes. Cependant, ce phénotype est transitoire et seulement légèrement lié aux modifications de la régulation transcriptionnelle de la machinerie autophagique. L'analyse de la fonction effectrice chez les plantes a montré que Avh195 retarde le développement de la mort cellulaire hypersensible, déclenchée par un éliciteur d’oomycète. Cette activité dépend de trois AIM sur cinq, ce qui renforce encore l’importance de l’interaction Avh195-ATG8 pour la fonction de l’effecteur. La surexpression stable d'Avh195 chez A. thaliana a permis de déterminer que l'effecteur n'altère pas les réponses immunitaires des plantes, mais favorise globalement le développement de l'agent pathogène, accélérant le passage de la biotrophie à la nécrotrophie au cours de l'infection. À notre connaissance, le travail présenté dans cette thèse représente la première preuve qu'un effecteur d’oomycète possède une activité transitoire, ciblant de manière non sélective la protéine ATG8 dans différents organismes photosynthétiques pour ralentir le flux autophagique, favorisant ainsi le mode de vie hémi-biotrophe d'un agent pathogène
The plant pathogen Phytophthora parasitica is an oomycete with devastating impact on both agriculture and natural ecosystems. As a hemi-biotrophic organism it infects the roots of plants first establishing an intimate contact with host cells (biotrophy) before killing them (necrotrophy) and completing its infection cycle. To control these processes, oomycetes secrete effector proteins, which are internalized in plant cells by a translocation motif (called RxLR-EER) to manipulate the physiology and the immune responses of the host. Studies of the molecular exchanges between Phytophthora parasitica and the plant that were conducted by the hosting laboratory led to the identification of an RxLR effector, designed to as Avh195. The amino acid sequence of the effector is characterized by the presence of five AIMs (ATG8 interacting motifs), that indicate a potential interaction with the autophagic core protein, ATG8. Avh195 colocalizes with the membrane-bound fraction of ATG8, and a yeast two-hybrid system, which allows to determine interactions between membrane proteins, confirmed a non-selective interaction between Avh195 and several ATG8 isoforms. The characterization of Avh195-dependent autophagy perturbation was carried out in the unicellular alga Chlamydomonas reinhardtii after generation of transgenic lines overexpressing the effector. Analyses by flow cytometry revealed that Avh195 does not modify the physiology and fitness of the alga, both under normal growth conditions and during rapamycin-induced autophagy. Transmission electron microscopy of cells revealed that the effector provokes a delay in the autophagic flux, manifested as a reduced coalescence and clearance of autophagic vacuoles and a strong accumulation of starch in chloroplasts. However, this phenotype was transient and only slightly related to modifications in the transcriptional regulation of the autophagic machinery. The analysis of effector function in planta showed that Avh195 delays the development of hypersensitive cell death, which is triggered by an oomycete elicitor. This cell death-delaying activity is dependent on three out of five AIMs, further consolidating the importance of the Avh195-ATG8 interaction for the function of the effector. The stable overexpression of Avh195 in A. thaliana allowed to determine that the effector does not impair plant defense responses, but overall promotes the development of the pathogen, accelerating the switch from biotrophy to necrotrophy during infection. To our knowledge, the work presented in this thesis represents the first evidence for an oomycete effector to possess a transitory activity, which targets in a non-selective manner the protein ATG8 in different organisms from the green lineage to slow down autophagic flux, thus promoting the hemibiotrophic life style of a pathogen
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Fancy, Nurun Nahar. "Role of S-nitrosylation in plant salt stress." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29509.

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Salinity stress is one of the main challenges for crop growth and production. The estimated loss of crop yield due to salinity stress is up to 20% worldwide each year. Plants have evolved an array of mechanisms to defend themselves against salinity stress. A key aspect of plant responses to salinity stress is the engagement of a nitrosative burst that results in nitric oxide (NO) accumulation. A major mechanism for the transfer of NO bioactivity is S-nitrosylation which is a modification of the reactive thiol group of a rare but highly active cysteine residue within a protein through the addition of a NO moiety to generate an S-nitrosothiol (SNO). S-nitrosylation can result in altered structure, function and cellular localisation of a protein. Our findings suggest that S-nitrosylation is a key regulator of plant responses to salinity stress. Glutathione (GSH), a tripeptide cellular antioxidant, is S-nitrosylated to form S-nitrosoglutathione (GSNO), which functions as a stable store of NO bioactivity. Cellular GSNO levels are directly controlled by S-nitrosoglutathione reductase (GSNOR), thereby, regulating global SNO levels indirectly. The absence of this gene results in high levels of SNOs. In Arabidopsis, previous research has shown that loss-of-function mutation in GSNOR1 results in pathogen susceptibility (Feechan et al., 2005). In our study, we investigated salt tolerance in gsnor1-3 plants. We have found that this line is salt sensitive at various stages of their life cycle. Interestingly, classical salt stress signalling pathways are fully functional in gsnor1-3 plants. We have also explored non-classical pathways involved in salt tolerance. Autophagy is a cellular catabolic process which is involved in the recycling and degradation of unwanted cellular materials under stressed and non-stressed conditions. We have demonstrated that gsnor1-3 plants have impaired autophagy during salt stress. An accumulation of the autophagy marker NBR1 supports the lack of autophagosome formation. We hypothesised that S-nitrosylation might regulate upstream nodes of autophagosome formation. Our study demonstrated that at least one key player involved in autophagosome biogenesis is regulated by S-nitrosylation. ATG7, an E1-like activating enzyme, which regulates ATG8-PE and ATG12-ATG5 ubiquitin like conjugation systems, is S-nitrosylated in vitro and in vivo. S-nitrosylation of ATG7 impairs its function in vitro. We showed that S-nitrosylation of ATG7 is mediated by GSNO. Interestingly, ATG7 is also transnitrosylated by thioredoxin (TRX), another important redox regulatory enzyme. We suggest that similar mechanisms might exist in planta. Finally, work in this study revealed that S-nitrosylation of Cys558 and Cys637 cause the inhibition of ATG7 function. In aggregate, this study revealed a novel mechanism for the redox-based regulation of autophagy during salt stress.
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Sumita, Takuya. "Studies on intracellular protein degradation pathways in plant fungal pathogens." Kyoto University, 2019. http://hdl.handle.net/2433/242706.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第21829号
農博第2342号
新制||農||1068(附属図書館)
学位論文||H31||N5201(農学部図書室)
京都大学大学院農学研究科地域環境科学専攻
(主査)教授 田中 千尋, 教授 本田 与一, 准教授 刑部 正博
学位規則第4条第1項該当
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Puleston, Daniel. "The role of autophagy in CD8plus T cell immunity." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:6cc5b853-4899-4de2-8924-71f7ee0659a1.

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Zhang, Zhu. "Exploration of the anticancer mechanisms of novel chemotherapeutic adjuvants involving autophagy and immune system reprogramming in the treatment of pancreatic cancer." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/755.

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Pancreatic cancer is known to be one of the most life-threatening cancers characterized by aggressive local invasion and distant metastasis. The high basal level of autophagy in pancreatic cancer may be responsible for the low chemotherapeutic drug response rate and poor disease prognosis. However, the clinical application of autophagy inhibitors was unsatisfactory due to their toxicity and minimal single-agent anticancer efficacy. Hence, oncologists begin to consider the tumor microenvironment when exploring new drug targets. In the present study, the anti-tumorigenic mechanisms of two major phytochemicals derived from Chinese medicinal herbs had been investigated against pancreatic cancer development. Calycosin is a bioactive isoflavonoid of the medicinal plant Astragalus membranaceus. Our results have shown that calycosin inhibited the growth of various pancreatic cancer cells both in vitro and in vivo by inducing cell cycle arrest and apoptosis. Alternatively, calycosin also facilitated MIA PaCa-2 pancreatic cancer cell migration in vitro and increased the expression of epithelial-mesenchymal transition (EMT) biomarkers in vivo. Further mechanistic study suggests that induction of the Raf/MEK/ERK pathway and facilitated polarization of M2 tumor-associated macrophage in the tumor microenvironment both contribute to the pro-metastatic potential of calycosin in pancreatic cancer. These events appear to be associated with calycosin-evoked activation of TGF-β signaling, which may explain the paradoxical drug actions due to the dual roles of TGF-β as both tumor suppressor and tumor promoter in pancreatic cancer development under different conditions. Isoliquiritigenin (ISL) is a chalcone obtained from the medicinal plant Glycyrrhiza glabra, which can be a precursor for chemical conversion to form calycosin. Results have shown that ISL decreased the growth and EMT of pancreatic cancer cells in vitro, probably due to modulation of autophagy. ISL-induced inhibition of autophagy subsequently promoted reactive oxygen species (ROS) production, leading to induction of apoptosis in pancreatic cancer cells. Such phenomenon also contributed to the synergistic growth-inhibitory effect in combined treatment with the orthodox chemotherapeutic drug 5-fluorouracil. In addition, ISL-induced tumor growth inhibition in vivo was further demonstrated in a tumor xenograft mice model of pancreatic cancer. ISL promoted apoptosis and inhibited autophagy in the tumor tissues. Study on immune cells indicates that ISL could reduce the number of myeloid-derived suppressor cells (MDSCs) both in tumor tissue and in peripheral blood, while CD4+ and CD8+ T cells were increased correspondingly. In vitro test has revealed that ISL inhibited the polarization of M2 macrophage along with its inhibition of autophagy in M2 macrophage. These immunomodulating effects of ISL had reversed the pro-invasive role of M2 macrophage in pancreatic cancer.In conclusion, calycosin acts as a "double-edged sword" on the growth and metastasis of pancreatic cancer, which may be related to the dual roles of TGF-β and its influence on the tumor microenvironment. Alternatively, ISL consistently inhibited the growth and metastatic drive of pancreatic cancer through regulation of autophagy and reprogramming of the immune system. The differential modes of action of these compounds have provided new insights in the development of effective pancreatic cancer treatment adjuvants.
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Milani, Manuela. "Cell stress response and hypoxia in breast cancer." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:74d3bf91-9888-4e9e-b5e1-7d5d2d476174.

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During severe hypoxia (<0.01% oxygen) the protein folding machinery becomes dysfunctional, resulting in the accumulation of unfolded proteins with consequent endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) and autophagy, a process involved in the physiological turnover of cytoplasmic components. The link between the UPR and autophagy is not clearly defined. The aim of this thesis is to investigate the role of the induction of UPR under severe hypoxia in tumour survival and resistance to therapy. The results of this research suggest that the activating transcription factor 4 (ATF4), a component of the PKR-like ER kinase (PERK) pathway, fundamental in the UPR, is required for the ER-stress induced upregulation of autophagy. Mechanisms other than hypoxia for UPR induction were investigated, using the proteasome inhibitor bortezomib (BZ). BZ treatment increased ATF4 protein levels in MCF7 cells, even transfected with short-interference RNA (siRNA) against the classical UPR activator PERK, suggesting that the proteasomal stabilization is likely the main mechanism for ATF4 protein accumulation. The induction of autophagy by BZ is dependent upon the upregulation of the microtubule-associated protein 1 light chain 3B (LC3B), an autophagy marker, by ATF4 and acts as a survival mechanism. Hypoxia, UPR and autophagy markers (such as Pimonidazole, carbonic anhydrases IX (CAIX), C/EBP homologous protein (CHOP) and LC3B) were evaluated by immunohistochemical approach in spheroids, xenografts models and breast cancer samples. CHOP immunohistochemical staining was performed in breast cancer sections from a series of patients. CHOP was expressed in cells surrounding necrotic areas. No correlation were found with clinical outcome and further studies are needed.
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Escamez, Sacha. "Xylem cells cooperate in the control of lignification and cell death during plant vascular development." Doctoral thesis, Umeå universitet, Institutionen för fysiologisk botanik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-115787.

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The evolutionary success of land plants was fostered by the acquisition of the xylem vascular tissue which conducts water and minerals upwards from the roots. The xylem tissue of flowering plants is composed of three main types of cells: the sap-conducting tracheary elements (TE), the fibres which provide mechanical support and the parenchyma cells which provide metabolic support to the tissue. Both the TEs and the fibres deposit thick polysaccharidic secondary cell walls (SCWs), reinforced by a rigid phenolic polymer called lignin. The cell walls of TEs form efficient water conducting hollow tubes after the TEs have undergone programmed cell death (PCD) and complete protoplast degradation as a part of their differentiation. The work presented in this thesis studied the regulation of TE PCD by characterizing the function of the candidate PCD regulator METACASPASE 9 (MC9) in Arabidopsis thaliana xylogenic cell suspensions. These cell suspensions can be externally induced to differentiate into a mix of TEs and parenchymatic non-TE cells, thus representing an ideal system to study the cellular processes of TE PCD. In this system, TEs with reduced expression of MC9 were shown to have increased levels of autophagy and to trigger the ectopic death of the non-TE cells. The viability of the non-TE cells could be restored by down-regulating autophagy specifically in the TEs with reduced MC9 expression. Therefore, this work showed that MC9 must tightly regulate the level of autophagy during TE PCD in order to prevent the TEs from becoming harmful to the non-TEs. Hence, this work demonstrated the existence of a cellular cooperation between the TEs and the surrounding parenchymatic cells during TE PCD. The potential cooperation between the TEs and the neighbouring parenchyma during the biosynthesis of lignin was also investigated. The cupin domain containing protein PIRIN2 was found to regulate TE lignification in a non-cell autonomous manner in Arabidopsis thaliana. More precisely, PIRIN2 was shown to function as an antagonist of positive transcriptional regulators of lignin biosynthetic genes in xylem parenchyma cells. Part of the transcriptional regulation by PIRIN2 involves chromatin modifications, which represent a new type of regulation of lignin biosynthesis. Because xylem constitutes the wood in tree species, this newly discovered regulation of non-cell autonomous lignification represents a potential target to modify lignin biosynthesis in order to overcome the recalcitrance of the woody biomass for the production of biofuels.
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Zayer, Adam. "Cellular models for characterisation of MINA53, a 2-oxoglutarate-dependent dioxygenase." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:ebd1dfcd-0c8e-4c87-9644-8ddfd9208456.

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2-0xoglutarate/Fe(II)-dependent dioxygenases (ZOG Oxygenases) are a relatively poorly characterised enzyme family that hydroxylate biological macromolecules to regulate a variety of essential cellular processes in mammals, including; chromatin remodeling, extra-cellular matrix formation and oxygen sensing. The work in this th esis focuses on a ZOG Oxygenase termed Myc-Induced Nuclear Antigen (MINAS3). This enzyme has been implicated in ribosome biogenesis and cell proliferation, and observed overexpressed in several tumour types, yet the identity afits substrate(s) and their role in cancer is unknown. The aims of the resea rch that has resulted in this thesis were to; (i) develop a cell model of MINAS3 enzyme activity, (ii) apply this model to study the role of MINAS3 activity in cell transformation and cancer, and (iii) discover novel cellular processes regulated by MINA53 activity. As such, I have created an isogenic cell model consisting of K-Ras-transformed MINAS3 knockout mouse embryonic fibroblasts (MEFs) reconstituted with either wildtype or enzyme-inactive MINAS3. Using this model I have shown that MINAS3 activity maintains normal levels of the large ribosomal subunit (60S), and suppresses anchorage-independent growth, autophagy and gene expression. These observations suggest the existence and involvement of one or more substrates. Indeed, proteomic and biochemical analyses in collaboration with the Schofield laboratory (Chemistry, Oxford) confirmed the identity of a MINA53 substrate, the 60S ribosomal protein Rp127a. Together we have shown that Rpl27a is abundantly hydroxylated, and that MINA53 is a histidinyJ hydroxylase; this represents the first discovery of a ribosomal oxygenase. The model developed here did not support a positive role for MINA53 in the transformation of MEFs. Rather it suggested that MINA53 can suppress transformation in some contexts, This prompted a wider investigation that demonstrated underexpression of MINA53 in several tumour types, and the presence of inactivating mutations in breast. ovarian and colon cancer. This thesis provides data supporting further research to understand the role of Rpl27a hydroxylation in the regulation of 60S biogenesis, autophagy and cancer. 2
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Books on the topic "Plant autophagy"

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Bassham, Diane C., and Jose L. Crespo, eds. Autophagy in plants and algae. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-477-3.

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Ramos, Jason. Intermittent Fasting Diabetes: Prevent and Reverse Diabetes and Learn How Autophagy and Keto Diet Can Help You Lose Weight. a Complete 101 Guide for Women and Men with Easy Meal Plans. Independently Published, 2019.

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Book chapters on the topic "Plant autophagy"

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Chen, Liang, Faqiang Li, and Shi Xiao. "Analysis of Plant Autophagy." In Methods in Molecular Biology, 267–80. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7262-3_24.

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Zeng, Hong-Yun, Ping Zheng, Ling-Yan Wang, He-Nan Bao, Sunil Kumar Sahu, and Nan Yao. "Autophagy in Plant Immunity." In Advances in Experimental Medicine and Biology, 23–41. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0606-2_3.

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Rodríguez, Milagros Collados, Katarzyna Zientara-Rytter, and Agnieszka Sirko. "Role of Autophagy in Plant Nutrient Deficiency." In Plant Ecophysiology, 171–203. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-10635-9_7.

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Cui, Xuefei, Jing Zheng, Jinxin Zheng, and Qingqiu Gong. "Study of Autophagy in Plant Senescence." In Methods in Molecular Biology, 299–306. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7672-0_23.

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Floyd, Brice E., Yunting Pu, Junmarie Soto-Burgos, and Diane C. Bassham. "To Live or Die: Autophagy in Plants." In Plant Programmed Cell Death, 269–300. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21033-9_11.

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Seay, Montrell, Andrew P. Hayward, Jeffrey Tsao, and S. P. Dinesh-Kumar. "Something Old, Something New: Plant Innate Immunity and Autophagy." In Current Topics in Microbiology and Immunology, 287–306. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00302-8_14.

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Husen, Azamal. "Cross Talk Between Autophagy and Hormones for Abiotic Stress Tolerance in Plants." In Plant Performance Under Environmental Stress, 1–15. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78521-5_1.

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Papini, Alessio. "Investigation of Morphological Features of Autophagy During Plant Programmed Cell Death." In Methods in Molecular Biology, 9–19. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7668-3_2.

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Ashrafizadeh, Milad, Shima Tavakol, Reza Mohammadinejad, Zahra Ahmadi, Habib Yaribeygi, Tannaz Jamialahmadi, Thomas P. Johnston, and Amirhossein Sahebkar. "Paving the Road Toward Exploiting the Therapeutic Effects of Ginsenosides: An Emphasis on Autophagy and Endoplasmic Reticulum Stress." In Pharmacological Properties of Plant-Derived Natural Products and Implications for Human Health, 137–60. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64872-5_12.

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Laureano-Marín, Ana M., Inmaculada Moreno, Ángeles Aroca, Irene García, Luis C. Romero, and Cecilia Gotor. "Regulation of Autophagy by Hydrogen Sulfide." In Gasotransmitters in Plants, 53–75. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40713-5_3.

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Conference papers on the topic "Plant autophagy"

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Peththa Thanthrige, Nipuni. "AtBAG4 interacts with NBR1 to promote chaperone-mediated autophagy and stress tolerance." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1052976.

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Akintayo, Oluwatoyosi F. "The Arabidopsis plasma membrane PSS1 protein conferring nhost immunity contributes to defense through autophagy following infection." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1053055.

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Yu, PEIFENG. "Dynamic Activity Regulation of the Ubiquitin-26S Proteasome System and Autophagy is Essential for Proper Seed Development." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1049094.

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Rabadanova, K. K., E. V. Tyutereva, K. S. Dobryakova, and O. V. Voitsekhovskaja. "The potassium role in the autophagy induction in salt stress in Arabidopsis thaliana." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-370.

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Murtuzova, A. V., K. K. Rabadanova, K. S. Dobryakova, E. V. Tyutereva, and O. V. Voitsekhovskaja. "The role of potassium in the regulation of constitutive and stress-induced autophagy in plants." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future. Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-299.

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Apollonov, V. I. "Regulation of autophagy, cell death and growth under salt stress in barley varieties with different salt tolerance." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-47.

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Minibayeva, F. V. "OXIDATIVE STRESS AND AUTOPHAGY IN PLANT CELLS: THE ROLE OF MITOCHONDRIA." In The Second All-Russian Scientific Conference with international participation "Regulation Mechanisms of Eukariotic Cell Organelle Functions". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-318-1-65-65.

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Zharova, D. A., A. I. Evkaykina, O. N. Boldina, O. V. Voitsekhovskaja, and E. V. Tyutereva. "Study of the role of autophagy in stress resistance and activation of astaxanthin biosynthesis in the microalga Haematococcus pluvialis." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-169.

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Sasanuma, I., N. Suzuki, and K. Saito. "Rose essential oils stimulate neural differentiation and autophagy in stem cells." In 67th International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA) in cooperation with the French Society of Pharmacognosy AFERP. © Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3400081.

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Wang, Xin-Ru. "The roles of autophagy in the interactions of a whitefly with a plant virus it transmits." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.112405.

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