Sulphide Resistance in the Cyanobacterium Microcystis aeruginosa: a Comparative Study of Morphology and Photosynthetic Performance Between the Sulphide-Resistant Mutant and the Wild-Type Strain

2015 ◽  
Vol 71 (4) ◽  
pp. 860-872 ◽  
Author(s):  
Elena Bañares-España ◽  
María del Mar Fernández-Arjona ◽  
María Jesús García-Sánchez ◽  
Miguel Hernández-López ◽  
Andreas Reul ◽  
...  
Keyword(s):  
Comparative Study ◽  
Microcystis Aeruginosa ◽  
Type Strain ◽  
Wild Type Strain ◽  
Resistant Mutant ◽  
Photosynthetic Performance ◽  
Wild Type

scholarly journals Impact of Inorganic Carbon Availability on Microcystin Production by Microcystis aeruginosa PCC 7806

2007 ◽  
Vol 73 (21) ◽  
pp. 6994-7002 ◽  
Author(s):  
Sabine J�hnichen ◽  
Tilo Ihle ◽  
Thomas Petzoldt ◽  
J�rgen Benndorf
Keyword(s):  
Microcystis Aeruginosa ◽  
Type Strain ◽  
Inorganic Carbon ◽  
Wild Type Strain ◽  
Light Cycle ◽  
Variable Fluorescence ◽  
Wild Type ◽  
Dark Light ◽  
Sodium Dependent ◽  
The Impact

ABSTRACT Batch culture experiments with the cyanobacterium Microcystis aeruginosa PCC 7806 were performed in order to test the hypothesis that microcystins (MCYSTs) are produced in response to a relative deficiency of intracellular inorganic carbon (Ci,i). In the first experiment, MCYST production was studied under increased Ci,i deficiency conditions, achieved by restricting sodium-dependent bicarbonate uptake through replacement of sodium bicarbonate in the medium with its potassium analog. The same experimental approach was used in a second experiment to compare the response of the wild-type strain M. aeruginosa PCC 7806 with its mcyB mutant, which lacks the ability to produce MCYSTs. In a third experiment, the impact of varying the Ci,i status on MCYST production was examined without suppressing the sodium-dependent bicarbonate transporter; instead, a detailed investigation of a dark-light cycle was performed. In all experiments, a relative Ci,i deficiency was indicated by an elevated variable fluorescence signal and led to enhanced phycocyanin cell quotas. Higher MCYST cell quotas (in the first and third experiments) and increased total (intracellular plus extracellular) MCYST production (in the first experiment) were detected with increased Ci,i deficiency. Furthermore, the MCYST-producing wild-type strain and its mcyB mutant showed basically the same response to restrained inorganic carbon uptake, with elevated variable fluorescence and phycocyanin cell quotas with increased Ci,i deficiency. The response of the wild type, however, was distinctly stronger and also included elevated chlorophyll a cell quotas. These differences indicate the limited ability of the mutant to adapt to low-Ci,i conditions. We concluded that MCYSTs may be involved in enhancing the efficiency of the adaptation of the photosynthetic apparatus to fluctuating inorganic carbon conditions in cyanobacterial cells.

scholarly journals A heat shock-resistant mutant of Saccharomyces cerevisiae shows constitutive synthesis of two heat shock proteins and altered growth.

1984 ◽  
Vol 99 (4) ◽  
pp. 1441-1450 ◽  
Author(s):  
H Iida ◽  
I Yahara
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Heat Shock ◽  
Type Strain ◽  
Wild Type Strain ◽  
Growth Control ◽  
Protein S ◽  
Resistant Mutant ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
Sulfur Starvation

A heat shock-resistant mutant of the budding yeast Saccharomyces cerevisiae was isolated at the mutation frequency of 10(-7) from a culture treated with ethyl methane sulfonate. Cells of the mutant are approximately 1,000-fold more resistant to lethal heat shock than those of the parental strain. Tetrad analysis indicates that phenotypes revealed by this mutant segregated together in the ratio 2+:2- from heterozygotes constructed with the wild-type strain of the opposite mating type, and are, therefore, attributed to a single nuclear mutation. The mutated gene in the mutant was herein designated hsr1 (heat shock response). The hsr1 allele is recessive to the HSR1+ allele of the wild-type strain. Exponentially growing cells of hsr1 mutant were found to constitutively synthesize six proteins that are not synthesized or are synthesized at reduced rates in HSR1+ cells unless appropriately induced. These proteins include one hsp/G0-protein (hsp48A), one hsp (hsp48B), and two G0-proteins (p73, p56). Heterozygous diploid (hsr1/HSR1+) cells do not synthesize the proteins constitutively induced in hsr1 cells, which suggests that the product of the HSR1 gene might negatively regulate the synthesis of these proteins. The hsr1 mutation also led to altered growth of the mutant cells. The mutation elongated the duration of G1 period in the cell cycle and affected both growth arrest by sulfur starvation and growth recovery from it. We discuss the problem of which protein(s) among those constitutively expressed in growing cells of the hsr1 mutant is responsible for heat shock resistance and alterations in the growth control.

scholarly journals Effect of Trehalose and Trehalose Transport on the Tolerance ofClostridium perfringensto Environmental Stress in a Wild Type Strain and Its Fluoroquinolone-Resistant Mutant

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Miseon Park ◽  
Wilfrid J. Mitchell ◽  
Fatemeh Rafii
Keyword(s):  
Environmental Stress ◽  
Type Strain ◽  
Wild Type Strain ◽  
Resistant Mutant ◽  
Defined Medium ◽  
Low Ph ◽  
Bacterial Cells ◽  
Chemically Defined Medium ◽  
Wild Type ◽  
Qrt Pcr

Trehalose has been shown to protect bacterial cells from environmental stress. Its uptake and osmoprotective effect inClostridium perfringenswere investigated by comparing wild typeC. perfringensATCC 13124 with a fluoroquinolone- (gatifloxacin-) resistant mutant. In a chemically defined medium, trehalose and sucrose supported the growth of the wild type but not that of the mutant. Microarray data and qRT-PCR showed that putative genes for the phosphorylation and transport of sucrose and trehalose (via phosphoenolpyruvate-dependent phosphotransferase systems, PTS) and some regulatory genes were downregulated in the mutant. The wild type had greater tolerance than the mutant to salts and low pH; trehalose and sucrose further enhanced the osmotolerance of the wild type to NaCl. Expression of the trehalose-specific PTS was lower in the fluoroquinolone-resistant mutant. Protection ofC. perfringensfrom environmental stress could therefore be correlated with the ability to take up trehalose.

scholarly journals Role of Microcystins in Poisoning and Food Ingestion Inhibition of Daphnia galeata Caused by the Cyanobacterium Microcystis aeruginosa

1999 ◽  
Vol 65 (2) ◽  
pp. 737-739 ◽  
Author(s):  
Thomas Rohrlack ◽  
Elke Dittmann ◽  
Manfred Henning ◽  
Thomas Börner ◽  
Johannes-Günter Kohl
Keyword(s):  
Microcystis Aeruginosa ◽  
Type Strain ◽  
Wild Type Strain ◽  
Ingestion Rate ◽  
Lethal Effect ◽  
Wild Type ◽  
Daphnia Galeata ◽  
Eutrophic Lakes ◽  
Microcystin Synthetase

ABSTRACT The effects of microcystins on Daphnia galeata, a typical filter-feeding grazer in eutrophic lakes, were investigated. To do this, the microcystin-producing wild-type strain Microcystis aeruginosa PCC7806 was compared with a mcy− PCC7806 mutant, which could not synthesize any variant of microcystin due to mutation of a microcystin synthetase gene. The wild-type strain was found to be poisonous toD. galeata, whereas the mcy− mutant did not have any lethal effect on the animals. Both variants of PCC7806 were able to reduce the Daphnia ingestion rate. Our results suggest that microcystins are the most likely cause of the daphnid poisoning observed when wild-type strain PCC7806 is fed to the animals, but these toxins are not responsible for inhibition of the ingestion process.

scholarly journals Controlling the hypermutation: Exploitation of the MutS protein in Pseudomonas aeruginosa

2020 ◽  
Vol 2 (7A) ◽  
Author(s):  
Yue Yuan On ◽  
Martin Welch
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Type Strain ◽  
Wild Type Strain ◽  
Resistant Mutant ◽  
Inducible Promoter ◽  
Wild Type ◽  
Cdna Analysis ◽  
In The Wild ◽  
Mismatch Recognition ◽  
Muts Gene

Pseudomonas aeruginosa infections commonly develop in individuals with cystic fibrosis (CF), and its adaptation in such an unfavourable condition is always found to be related to hypermutation. In fact, most of the hypermutation is due to the defects in mutS gene which involves in the mismatch repair mechanism, causing the acceleration of mutation rate and adaptive evolution. In order to rheostatically express the MutS protein and achieve “hypomutation” (in which the rate of mutation is lower than that of wild type strain), an exogenous mutS gene with rhamnose-inducible promoter was cloned into MPAO1 mutS::Tn mutant strain. Present findings demonstrate that this system is tightly-controlled and stable, with less rifampicin-resistant mutant frequency and more fluorescence intensity from a GFP-tagged MutS expressing cells were observed when the concentration of the inducer increases. Interestingly, the results from Western blot analysis show that less MutS protein is required to suppress hypermutation in the wild type strain, as compared to our construct that behaves similar to the wild type but obviously needs more MutS expression to achieve such state. This indicates that the exogenous MutS might be lacking of other important protein to work efficiently in mismatch recognition. Therefore, based on our cDNA analysis, we found that fdxA gene next to the mutS gene is in the same operon, which could suggest that they might be functionally related in the DNA repair machinery.

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