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Dynein in Intraflagellar Transport
Published in Keiko Hirose, Handbook of Dynein, 2019
Proteins that depend on retrograde IFT for flagellar export are likely to bind to the IFT particles or the BBSome rather than directly to IFT dynein. BBS mutants in Chlamydomonas accumulate phospholipase D (PLD) which is efficiently banned from wild-type cilia [46]. Similarly, non-ciliary proteins accumulate in the outer segment of rod cells in Bbs−/− mutant mice and certain G-protein coupled receptors (GPCRs) accumulate in Bbs mutant cilia [17, 52]. PLD also accumulates in flagella of the IFT dynein mutant dhc1b-2 and of fla17-1, expressing a truncated version of the IFT-A particle protein IFT139. The BBSome appears to function as a cargo adapter to allow protein export via IFT dynein-dependent retrograde IFT. Interestingly, PLD also accumulates in cilia when IFT is switched off using the fast acting kinesin-2 mutant fla10-1 [45]. This suggests that PLD can enter cilia by diffusion but requires active retrograde IFT to be removed from cilia. Retrograde IFT could function as a scavenger removing cell body proteins entering cilia by diffusion from the organelle.
Regulation of Osmolytes Syntheses and Improvement of Abiotic Stress Tolerance in Plants
Published in Hasanuzzaman Mirza, Nahar Kamrun, Fujita Masayuki, Oku Hirosuke, Tofazzal M. Islam, Approaches for Enhancing Abiotic Stress Tolerance in Plants, 2019
Ambuj Bhushan Jha, Pallavi Sharma
Thiery et al. (2004) reported the possible role of phospholipase D besides calcium and ABA for the regulation of proline synthesis. Proline accumulation is negatively controlled by phospholipase D under non-stressed conditions (Knight et al., 1997; Parre et al., 2007). Phospholipase D itself has been suggested to be regulated by calcium. The data also indicated that the application of primary butyl alcohols enhanced the proline responsiveness of seedlings to mild hyperosmotic stress. Higher proline responsiveness was observed to hyperosmotic stress when phospholipase D was abolished (Kavi Kishor et al., 2005). VPS34, class-III phosphatidylinositol 3-kinase (PI3K), which catalyzes synthesis of phosphatidylinositol 3-phosphate (PI3P) from phosphatidylinositol, also controls proline metabolism (Leprince et al., 2015) and this was confirmed by use of the PI3K inhibitor, LY294002, which adversely affects PI 3P levels and reduced proline, amino acids and sugars accumulation in salt-stressed A. thaliana seedlings. Further, proline accumulation was positively correlated with transcript level of P5CS1 and negatively correlated with transcript and protein levels of ProDH1. Induced expression of ProDH1 in a pi3k-hemizygous mutant indicates the role of PI3K for ProDH1 regulation and thus proline catabolism (Leprince et al., 2015).
Biotransformations in Deep Eutectic Solvents
Published in Pedro Lozano, Sustainable Catalysis in Ionic Liquids, 2018
Vicente Gotor-Fernández, Caroline Emilie Paul
In this last section, a few conventional catalyzed reactions are covered which occurred in DES-containing systems. Recently, the phospholipase D-catalyzed transphophatidylation of phosphatidylcholine has been reported with 6 equiv. of L-serine for the synthesis of phosphatidylserine, phospholipid with interesting properties to rejuvenate brain cell membranes and increase acetylcholine levels in the brain (Yang and Duan 2016). The biotransformation was attempted in various DESs with 0.5% v/v water, yielding over 90% yield employing ChCl:EG (1:2, 90.3% after 7 h) or ChCl:Gly (1:2, 92.1% after 12 h) at 40°C. In addition, 81% of the original enzymatic activity was maintained after nine reuses when the reaction was carried under optimal conditions in ChCl:EG.
Increasing cannabis use and importance as an environmental contaminant mixture and associated risks to exposed biota: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Emily K. C. Kennedy, Genevieve A. Perono, Dion B. Nemez, Alison C. Holloway, Philippe J. Thomas, Robert Letcher, Chris Marvin, Jorg Stetefeld, Jake Stout, Oliver Peters, Vince Palace, Gregg Tomy
While numerous constituents can be derived from C. sativa, cannabinoids can also be synthesized endogenously (endocannabinoids) or derived synthetically (Lu & Mackie, 2016). Of the more than 100 active cannabinoids identified, each has the capacity to modulate the endocannabinoid system (ECS), which is a network of cannabinoid receptors, cannabinoid ligands (i.e., phytocannabinoids, endocannabinoids and synthetic cannabinoids) and enzymes involved in endocannabinoid synthesis (e.g., N-acyl-phosphatidyl-ethanolamine-specific phospholipase D, NAPE-PLD; diacylglycerol lipases, DAGL) and degradation (e.g., fatty acid amide hydrolase, FAAH; monoacylglycerol lipase, MAGL) (Lu & Mackie, 2016). Endocannabinoids are categorized into amides and esters. The most studied endocannabinoids are anandamide (AEA) and 2-arachydonyl glycerol (2-AG); their different modes of modulation are reviewed in detail elsewhere (Reviewed in: (Lu & Mackie, 2016)). AEA, 2-AG and other endocannabinoids function as retrograde messengers, modulating neurotransmitter release after they are synthesized and released postsynaptically (Kano et al., 2009; Katona & Freund, 2012).
Molecular toxicology and carcinogenesis of fumonisins: a review
Published in Journal of Environmental Science and Health, Part C, 2020
Ruth Nabwire Wangia-Dixon, Kizito Nishimwe
The disruption results in accumulation of intracellular free sphinganine, which is linked to alteration of the sphinganine to sphingosine ratio and forms a basis for a biomarker of fumonisin.41 Furthermore, a close relationship on the role of sphinganine accumulation on liver and kidney toxicity has been widely studied and discussed.54,55 Once accumulated, free sphingolipid bases persist in the kidneys much longer than fumonisin B1, which supports the claim that the kidneys are ultimately more sensitive to fumonisin toxicity compared to other organs.12,28,55 Overall, fumonisin-induced increases in free sphingolipid bases and toxicity are both reversible, and elimination of free Sphinganine was faster in liver compared to kidneys of rodents.12,28,55 A portion of the accumulated Sphinganine is metabolized to Sa- 1- phosphate (SaP) and then cleaved into a fatty aldehyde and ethanolamine phosphate.11,56 Sphingolipids are involved in signaling pathways, cell recognition and modulating interactions with receptors and integrin.11,13,57 Other consequences associated with disruption of de novo synthesis pathway of sphingolipid metabolism include inhibition of the protein kinase C, activation of phospholipase D, inhibition of Na+/K+ATPase and induction of dephosphorylation of retinoblastoma protein.11,58,59 Ultimately, once complex sphingolipid are depleted, inhibition of cell growth occurs and ultimately induction of apoptosis.59
Longitudinal metabolic alterations in plasma of rats exposed to low doses of high linear energy transfer radiation
Published in Journal of Environmental Science and Health, Part C, 2021
Tixieanna Dissmore, Andrew G DeMarco, Meth Jayatilake, Michael Girgis, Shivani Bansal, Yaoxiang Li, Khyati Mehta, Vijayalakshmi Sridharan, Kirandeep Gill, Sunil Bansal, John B Tyburski, Amrita K Cheema
Complex cellular responses triggered by exposure to non-lethal doses of ionizing radiation may lead to changes in metabolomic profiles depending on radiation type and dose.18–22 In this study, we report the results from a rat model aimed at delineating longitudinal alterations in the plasma metabolome after exposure to 0.5 Gy of 1H (250 MeV) or 16O (600 MeV/n) radiation. The dysregulated metabolites included certain classes of lipids such as phosphatidylethanolamine (PE), ceramide, sphingomyelin (SM) and lysophosphatidic acid (LPA). Pro-inflammatory cytokines and oxidative stress may stimulate the generation of SMs, from the ceramide response to sphingomyelin synthase in the Golgi apparatus.23 Dysregulation observed in SM(24:1) at the 3-month time point may indicate some degree of neuronal damage.24 Additionally, we found a significant increase in eicosapentaenoyl PAF C-16 after exposure to 0.5 Gy of 1H at 12 the month time point, which may be because of ionizing radiation-mediated oxidation of phospholipids. Radiation-induced peroxidation of fatty acids may indicate cellular damage at various levels.25,26 Lastly, we observed decreased levels of LPA(18:0) after exposure to 1H and 16O at 12 months. Previously it has been reported that inflammatory prostaglandins Phosphatidylcholine (PC) generates lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA) through the actions of Pla2) and phospholipase D (Pld) that is further converted to Phosphatidic acid (PA). Decreased levels of LPA may suggest increased levels of PA that can directly stimulate G protein-coupled receptor activation of mTor through resulting in increased cell proliferation.27