scholarly journals Homologous transformation ofTrichoderma hamatumwith an endochitinase encoding gene, resulting in increased levels of chitinase activity

1998 ◽  
Vol 165 (2) ◽  
pp. 247-252 ◽  
Author(s):  
Gábor Giczey ◽  
Zoltán Kerényi ◽  
Géza Dallmann ◽  
László Hornok
Gene ◽  
1990 ◽  
Vol 90 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Michael P. Whitehead ◽  
Sarah Jane Gurr ◽  
Carolyn Grieve ◽  
Shiela E. Unkles ◽  
David Spence ◽  
...  

2016 ◽  
Vol 106 (9) ◽  
pp. 971-977 ◽  
Author(s):  
Huiyong Xu ◽  
Hongfu Chen ◽  
Yuemao Shen ◽  
Liangcheng Du ◽  
Shan-Ho Chou ◽  
...  

Lysobacter enzymogenes is a gram-negative bacterial biological control agent that produces abundant extracellular enzymes capable of degrading the cell walls of fungal pathogens. In strain OH11, an isolate from China, the global regulator LeClp controls the production of extracellular chitinase by regulating the transcription of the chitinase-encoding gene chiA. Using a combination of bioinformatic, genetic, and biochemical methods, we show that LeClp regulates chiA transcription by directly binding to the chiA promoter region. Although LeClp appears to be important in this role, it is not the sole regulator of chiA transcription. Furthermore, the sequence analysis of putative LeClp binding sites indicated that the LeClp homolog could be involved in the regulation of extracellular chitinase production in diverse Lysobacter spp. by a mechanism similar to that in L. enzymogenes. Our findings present new insights into the molecular mechanism of LeClp in controlling extracellular chitinase activity, providing a fundamental road to elucidate how LeClp regulates the production of other extracellular lytic enzymes in L. enzymogenes.


2001 ◽  
Vol 120 (5) ◽  
pp. A162-A162
Author(s):  
A KUTUP ◽  
S HOSCH ◽  
S PAPE ◽  
P SCHEUNEMANN ◽  
W KNOEFEL ◽  
...  

2020 ◽  
pp. 23-25
Author(s):  
A. Venger ◽  
O. Venger ◽  
Y. Vasina ◽  
I. Zhuravlov ◽  
I. Kholodnitskiy ◽  
...  

Plant Omics ◽  
2017 ◽  
Vol 10 (05) ◽  
pp. 247-251 ◽  
Author(s):  
Yurnaliza ◽  
◽  
Rizkita Rachmi Esyanti ◽  
Agus Susanto ◽  
I Nyoman Pugeg Aryantha ◽  
...  

2021 ◽  
Vol 193 (9) ◽  
Author(s):  
Damjana Drobac Backović ◽  
Nada Tokodi ◽  
Zoran Marinović ◽  
Jelena Lujić ◽  
Tamara Dulić ◽  
...  

AbstractCyanobacteria are important members of lake plankton, but they have the ability to form blooms and produce cyanotoxins and thus cause a number of adverse effects. Freshwater ecosystems around the world have been investigated for the distribution of cyanobacteria and their toxins and the effects they have on the ecosystems. Similar research was performed on the Fehérvárcsurgó reservoir in Hungary during 2018. Cyanobacteria were present and blooming, and the highest abundance was recorded in July (2,822,000 cells/mL). The species present were Aphanizomenon flos-aquae, Microcystis flos-aquae, Microcystis wesenbergii, Cuspidothrix issatschenkoi, Dolichospermum flos-aquae, and Snowella litoralis. In July and September, the microcystin encoding gene mcyE and the saxitoxin encoding gene sxtG were amplified in the biomass samples. While a low concentration of microcystin-RR was found in one water sample from July, analyses of Abramis brama and Carassius gibelio caught from the reservoir did not show the presence of the investigated microcystins in the fish tissue. However, several histopathological changes, predominantly in gills and kidneys, were observed in the fish, and the damage was more severe during May and especially July, which coincides with the increase in cyanobacterial biomass during the summer months. Cyanobacteria may thus have adverse effects in this ecosystem.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ruiqi Wang ◽  
Kun Li ◽  
Jifang Yu ◽  
Jiaoyu Deng ◽  
Yaokai Chen

AbstractPrevious studies showed that mutation of folC caused decreased expression of the dihydropteroate synthase encoding gene folP2 in Mycobacterium tuberculosis (M. tuberculosis). We speculated that mutation of folC in M. tuberculosis might affect the susceptibility to sulfamethoxazole (SMX). To prove this, 53 clinical isolates with folC mutations were selected and two folC mutants (I43A, I43T) were constructed based on M. tuberculosis H37Ra. The results showed that 42 of the 53 clinical isolates (79.2%) and the two lab-constructed folC mutants were more sensitive to SMX. To probe the mechanism by which folC mutations make M. tuberculosis more sensitive to SMX, folP2 was deleted in H37Ra, and expression levels of folP2 were compared between H37Ra and the two folC mutants. Although deletion of folP2 resulted in increased susceptibility to SMX, no difference in folP2 expression was observed. Furthermore, production levels of para-aminobenzoic acid (pABA) were compared between the folC mutants and the wild-type strain, and results showed that folC mutation resulted in decreased production of pABA. Taken together, we show that folC mutation leads to decreased production of pABA in M. tuberculosis and thus affects its susceptibility to SMX, which broadens our understanding of mechanisms of susceptibilities to antifolates in this bacterium.


Genetics ◽  
1996 ◽  
Vol 144 (4) ◽  
pp. 1455-1462
Author(s):  
José L Barra ◽  
Mario R Mautino ◽  
Alberto L Rosa

eth-1r a thermosensitive allele of the Neurospora crassa S-adenosylmethionine (AdoMet) synthetase gene that confers ethionine resistance, has been cloned and sequenced. Replacement of an aspartic amino acid residue (D48 → N48), perfectly conserved in prokaryotic, fungal and higher eukaryotic AdoMet synthetases, was found responsible for both thermosensitivity and ethionine resistance conferred by eth-1r. Gene fusion constructs, designed to overexpress eth-1r in vivo, render transformant cells resistant to ethionine. Dominance of ethionine resistance was further demonstrated in eth-1  +/eth-1r partial diploids carrying identical gene doses of both alleles. Heterozygous eth-1  +/eth-1r cells have, at the same time, both the thermotolerance conferred by eth-1  + and the ethionine-resistant phenotype conferred by eth-1r. AdoMet levels and AdoMet synthetase activities were dramatically decreased in heterozygous eth-1  +/eth-1r cells. We propose that this negative effect exerted by eth-1r results from the in vivo formation of heteromeric eth-1  +/eth-1r AdoMet synthetase molecules.


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