scholarly journals High-Light-Induced Stress Activates Lipid Deacylation at the Sn-2 Position in the Cyanobacterium Synechocystis sp. PCC 6803

Author(s):  
Kouji Kojima ◽  
Ui Matsumoto ◽  
Sumie Keta ◽  
Kenji Nakahigashi ◽  
Kazutaka Ikeda ◽  
...  

Abstract Cyanobacterial mutants defective in acyl-acyl carrier protein synthetase (Aas) produce free fatty acids (FFAs) because the FFAs generated by deacylation of membrane lipids cannot be recycled. An engineered Aas-deficient mutant of Synechocystis sp. PCC 6803 grew normally under low-light (LL) conditions (50 µmol photons m-2 s-1) but was unable to sustain growth under high-light (HL) conditions (400 µmol photons m-2 s-1), revealing a crucial role of Aas in survival under the HL conditions. Several-times larger amounts of FFAs were produced by HL-exposed cultures than LL-grown cultures. Palmitic acid accounted for ~85% of total FFAs in HL-exposed cultures, while C18 fatty acids constituted ~80% of the FFAs in LL-grown cultures. Since C16 fatty acids are esterified to the sn-2 position of lipids in the Synechocystis species, it was deduced that HL irradiation activated deacylation of lipids at the sn-2 position. Heterologous expression of FarB, the FFA exporter protein of Neisseria lactamica, prevented intracellular FFA accumulation and rescued the growth defect of the mutant under HL, indicating that intracellular FFA was the cause of growth inhibition. FarB expression also decreased the per-cell yield of FFA under HL by 90% and decreased the proportion of palmitic acid to ~15% of total FFA. These results indicated that the HL-induced lipid deacylation is triggered not by strong light per se but by HL-induced damage to the cells. It was deduced that there is a positive feedback loop between HL-induced damage and lipid deacylation, which is lethal unless FFA accumulation is prevented by Aas.

2021 ◽  
Vol 22 (19) ◽  
pp. 10432
Author(s):  
Haruhiko Jimbo ◽  
Koki Yuasa ◽  
Kensuke Takagi ◽  
Takashi Hirashima ◽  
Sumie Keta ◽  
...  

Free fatty acids (FFAs) are generated by the reaction of lipases with membrane lipids. Generated polyunsaturated fatty acids (PUFAs) containing more than two double bonds have toxic effects in photosynthetic organisms. In the present study, we examined the effect of exogenous FFAs in the growth medium on the activity of photosystem II (PSII) under strong light in the cyanobacterium Synechocystis sp. PCC 6803 (Synechocystis). PUFAs but not monounsaturated fatty acids accelerated the rate of photodamage to PSII by inactivating electron transfer at the oxygen-evolving complex. Moreover, supplemented PUFAs were specifically incorporated into the sn-2 position of phosphatidylglycerol (PG), which usually contains C16 fatty acids at the sn-2 position in Synechocystis cells. The disruption of the gene for an acyl-ACP synthetase reduced the effect of PUFAs on the photoinhibition of PSII. Thus, the specific incorporation of PUFAs into PG molecules requires acyl-ACP synthetase and leads to an unstable PSII, thereby accelerating photodamage to PSII. Our results are a breakthrough into elucidating the molecular mechanism of the toxicity of PUFAs to photosynthetic organisms.


2000 ◽  
Vol 28 (6) ◽  
pp. 628-630 ◽  
Author(s):  
I. Suzuki ◽  
D. A. Los ◽  
N. Murata

When cells of the cyanobacterium Synechocystis sp. PCC 6803 are exposed to a low temperature, genes for fatty acid desaturases are expressed with resultant increases in the degree of unsaturation of fatty acids in membrane lipids. However, the sensor and transducers of low-temperature signals had not yet been identified. In order to identify these components we applied to the cyanobacterium Synechocystis sp. PCC 6803 the systematic disruption of all 43 putative genes for histidine kinases and random mutagenesis of the whole genome in conjunction with screening by the transcriptional activity of the promoter of the desB gene for the ω 3 desaturase. This allowed us to identify two histidine kinases and a response regulator as components of the perception and transduction of low-temperature signals for the expression of genes for fatty acid desaturases.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Anushree Bachhar ◽  
Jiri Jablonsky

AbstractPhosphoketolase (PKET) pathway is predominant in cyanobacteria (around 98%) but current opinion is that it is virtually inactive under autotrophic ambient CO2 condition (AC-auto). This creates an evolutionary paradox due to the existence of PKET pathway in obligatory photoautotrophs. We aim to answer the paradox with the aid of bioinformatic analysis along with metabolic, transcriptomic, fluxomic and mutant data integrated into a multi-level kinetic model. We discussed the problems linked to neglected isozyme, pket2 (sll0529) and inconsistencies towards the explanation of residual flux via PKET pathway in the case of silenced pket1 (slr0453) in Synechocystis sp. PCC 6803. Our in silico analysis showed: (1) 17% flux reduction via RuBisCO for Δpket1 under AC-auto, (2) 11.2–14.3% growth decrease for Δpket2 in turbulent AC-auto, and (3) flux via PKET pathway reaching up to 252% of the flux via phosphoglycerate mutase under AC-auto. All results imply that PKET pathway plays a crucial role under AC-auto by mitigating the decarboxylation occurring in OPP pathway and conversion of pyruvate to acetyl CoA linked to EMP glycolysis under the carbon scarce environment. Finally, our model predicted that PKETs have low affinity to S7P as a substrate.


2018 ◽  
Vol 60 (2) ◽  
pp. 367-375 ◽  
Author(s):  
Hiroko Takahashi ◽  
Yuri Kusama ◽  
Xinxiang Li ◽  
Shinichi Takaichi ◽  
Yoshitaka Nishiyama

2012 ◽  
Vol 159 (2) ◽  
pp. 606-617 ◽  
Author(s):  
Simon von Berlepsch ◽  
Hans-Henning Kunz ◽  
Susanne Brodesser ◽  
Patrick Fink ◽  
Kay Marin ◽  
...  

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