scholarly journals Influence of Different Light Regimes on the Mycoparasitic Activity and the Production of the Secondary Metabolite 6-Pentyl-α-Pyrone in Two Strains of Trichoderma Atroviride

2020 ◽  
Author(s):  
Dubraska Moreno-Ruiz ◽  
Alessandro Fuchs ◽  
Kristina Missbach ◽  
Rainer Schuhmacher ◽  
Susanne Zeilinger
Keyword(s):  
Secondary Metabolite ◽  
Green Light ◽  
Inhibitory Effect ◽  
Trichoderma Atroviride ◽  
Wild Type ◽  
Complete Darkness ◽  
Light Regimes ◽  
Encoding Gene ◽  
Type Strains ◽  
Strain Dependent

The ascomycete Trichoderma atroviride is well known for its mycoparasitic lifestyle. Similar to other organisms, light is an important cue for T. atroviride. However, besides triggering of conidiation, little is known on the physiological responses of T. atroviride to light. In this study, we analyzed how cultivation under different light wavelengths and regimes impacted the behavior of two T. atroviride wild-type strains, IMI206040 and P1. While colony extension of both strains was slightly affected by light, massive differences in the photoconidation response between the two strains became evident. T. atroviride P1 colonies conidiated under all conditions tested including growth in complete darkness, while IMI206040 required white, blue or green light to trigger asexual reproduction. Interestingly, deletion of the stress-activated MAP kinase-encoding gene tmk3 abolished the ability of strain P1 to conidiate in red and yellow light as well as in darkness. Furthermore, light-dependent differences in the mycoparasitic activity of T. atroviride and in the biosynthesis of the secondary metabolite 6-pentyl--pyrone (6-PP) became evident. 6-PP production was highest upon dark incubation while light, especially exposure to white light as light/dark cycles, had an inhibitory effect on its biosynthesis. We conclude that the response of T. atroviride to light is strain-dependent and impacts differentiation, mycoparasitism and 6-PP production and hence should be considered in experiments testing the mycoparasitic activity of these fungi.

scholarly journals Influence of Different Light Regimes on the Mycoparasitic Activity and 6-Pentyl-α-pyrone Biosynthesis in Two Strains of Trichoderma atroviride

Pathogens ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 860
Author(s):  
Dubraska Moreno-Ruiz ◽  
Alessandro Fuchs ◽  
Kristina Missbach ◽  
Rainer Schuhmacher ◽  
Susanne Zeilinger
Keyword(s):  
Green Light ◽  
Inhibitory Effect ◽  
Trichoderma Atroviride ◽  
Wild Type ◽  
Complete Darkness ◽  
Yellow Light ◽  
Light Regimes ◽  
Encoding Gene ◽  
Type Strains ◽  
Strain Dependent

The ascomycete Trichoderma atroviride is well known for its mycoparasitic lifestyle. Similar to other organisms, light is an important cue for T. atroviride. However, besides triggering of conidiation, little is known on the physiological responses of T. atroviride to light. In this study, we analyzed how cultivation under different light wavelengths and regimes impacted the behavior of two T. atroviride wild-type strains: IMI206040 and P1. While colony extension of both strains was slightly affected by light, massive differences in their photoconidation responses became evident. T. atroviride P1 colonies conidiated under all conditions tested including growth in complete darkness, while IMI206040 required white, blue or green light to trigger asexual reproduction. Interestingly, deletion of the stress-activated MAP kinase-encoding gene tmk3 abolished the ability of strain P1 to conidiate in red and yellow light as well as in darkness. Furthermore, light-dependent differences in the mycoparasitic activity and in the biosynthesis of the secondary metabolite 6-pentyl-α-pyrone (6-PP) became evident. 6-PP production was highest upon dark incubation, while light, especially exposure to white light as light/dark cycles, had an inhibitory effect on its biosynthesis. We conclude that the response of T. atroviride to light is strain-dependent and impacts differentiation, mycoparasitism, and 6-PP production; hence, this should be considered in experiments testing the mycoparasitic activity of these fungi.

scholarly journals Prion Strain-Dependent Differences in Conversion of Mutant Prion Proteins in Cell Culture

2006 ◽  
Vol 80 (16) ◽  
pp. 7854-7862 ◽  
Author(s):  
Ryuichiro Atarashi ◽  
Valerie L. Sim ◽  
Noriyuki Nishida ◽  
Byron Caughey ◽  
Shigeru Katamine
Keyword(s):  
Prion Protein ◽  
Prion Proteins ◽  
Basic Amino Acid ◽  
Inhibitory Effect ◽  
Wild Type ◽  
Prion Strain ◽  
Potent Inhibitory Effect ◽  
Scrapie Strain ◽  
Infected Cells ◽  
Strain Dependent

ABSTRACT Although the protein-only hypothesis proposes that it is the conformation of abnormal prion protein (PrPSc) that determines strain diversity, the molecular basis of strains remains to be elucidated. In the present study, we generated a series of mutations in the normal prion protein (PrPC) in which a single glutamine residue was replaced with a basic amino acid and compared their abilities to convert to PrPSc in cultured neuronal N2a58 cells infected with either the Chandler or 22L mouse-adapted scrapie strain. In mice, these strains generate PrPSc of the same sequence but different conformations, as judged by infrared spectroscopy. Substitutions at codons 97, 167, 171, and 216 generated PrPC that resisted conversion and inhibited the conversion of coexpressed wild-type PrP in both Chandler-infected and 22L-infected cells. Interestingly, substitutions at codons 185 and 218 gave strain-dependent effects. The Q185R and Q185K PrP were efficiently converted to PrPSc in Chandler-infected but not 22L-infected cells. Conversely, Q218R and Q218H PrP were converted only in 22L-infected cells. Moreover, the Q218K PrP exerted a potent inhibitory effect on the conversion of coexpressed wild-type PrP in Chandler-infected cells but had little effect on 22L-infected cells. These results show that two strains with the same PrP sequence but different conformations have differing abilities to convert the same mutated PrPC.

scholarly journals The GNAQ T96S Mutation Affects Cell Signaling and Enhances the Oncogenic Properties of Hepatocellular Carcinoma

2021 ◽  
Vol 22 (6) ◽  
pp. 3284
Author(s):  
Eugene Choi ◽  
Sung Jean Park ◽  
Gunhee Lee ◽  
Seung Kew Yoon ◽  
Minho Lee ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Expression Vector ◽  
Signal Transduction Pathway ◽  
Inhibitory Effect ◽  
The Cancer Genome Atlas ◽  
Treatment Modalities ◽  
Protein Signaling ◽  
Wild Type ◽  
Anchorage Independent Growth ◽  
Mapk Pathways

Hepatocellular carcinoma (HCC), the most common malignant tumor in the liver, grows and metastasizes rapidly. Despite advances in treatment modalities, the five-year survival rate of HCC remains less than 30%. We sought genetic mutations that may affect the oncogenic properties of HCC, using The Cancer Genome Atlas (TCGA) data analysis. We found that the GNAQ T96S mutation (threonine 96 to serine alteration of the Gαq protein) was present in 12 out of 373 HCC patients (3.2%). To examine the effect of the GNAQ T96S mutation on HCC, we transfected the SK-Hep-1 cell line with the wild-type or the mutant GNAQ T96S expression vector. Transfection with the wild-type GNAQ expression vector enhanced anchorage-independent growth, migration, and the MAPK pathways in the SK-Hep-1 cells compared to control vector transfection. Moreover, cell proliferation, anchorage-independent growth, migration, and the MAPK pathways were further enhanced in the SK-Hep-1 cells transfected with the GNAQ T96S expression vector compared to the wild-type GNAQ-transfected cells. In silico structural analysis shows that the substitution of the GNAQ amino acid threonine 96 with a serine may destabilize the interaction between the regulator of G protein signaling (RGS) protein and GNAQ. This may reduce the inhibitory effect of RGS on GNAQ signaling, enhancing the GNAQ signaling pathway. Single nucleotide polymorphism (SNP) genotyping analysis for Korean HCC patients shows that the GNAQ T96S mutation was found in only one of the 456 patients (0.22%). Our data suggest that the GNAQ T96S hotspot mutation may play an oncogenic role in HCC by potentiating the GNAQ signal transduction pathway.

scholarly journals Identification ofvib-1, a Locus Involved in Vegetative Incompatibility Mediated byhet-cinNeurospora crassa

Genetics ◽  
2002 ◽  
Vol 162 (1) ◽  
pp. 89-101 ◽  
Author(s):  
Qijun Xiang ◽  
N Louise Glass
Keyword(s):  
Acid Phosphatase ◽  
Recognition System ◽  
Deletion Mutants ◽  
Wild Type ◽  
Vegetative Incompatibility ◽  
Death Rates ◽  
Self Recognition ◽  
Allelic Differences ◽  
Native Gel ◽  
Type Strains

AbstractA non-self-recognition system called vegetative incompatibility is ubiquitous in filamentous fungi and is genetically regulated by het loci. Different fungal individuals are unable to form viable heterokaryons if they differ in allelic specificity at a het locus. To identify components of vegetative incompatibility mediated by allelic differences at the het-c locus of Neurospora crassa, we isolated mutants that suppressed phenotypic aspects of het-c vegetative incompatibility. Three deletion mutants were identified; the deletions overlapped each other in an ORF named vib-1 (vegetative incompatibility blocked). Mutations in vib-1 fully relieved growth inhibition and repression of conidiation conferred by het-c vegetative incompatibility and significantly reduced hyphal compartmentation and death rates. The vib-1 mutants displayed a profuse conidiation pattern, suggesting that VIB-1 is a regulator of conidiation. VIB-1 shares a region of similarity to PHOG, a possible phosphate nonrepressible acid phosphatase in Aspergillus nidulans. Native gel analysis of wild-type strains and vib-1 mutants indicated that vib-1 is not the structural gene for nonrepressible acid phosphatase, but rather may regulate nonrepressible acid phosphatase activity.

scholarly journals HET-E and HET-D Belong to a New Subfamily of WD40 Proteins Involved in Vegetative Incompatibility Specificity in the Fungus Podospora anserina

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 71-81
Author(s):  
Eric Espagne ◽  
Pascale Balhadère ◽  
Marie-Louise Penin ◽  
Christian Barreau ◽  
Béatrice Turcq
Keyword(s):  
Genetic Difference ◽  
Podospora Anserina ◽  
Wild Type ◽  
Incompatible Interaction ◽  
Vegetative Incompatibility ◽  
Repeat Domain ◽  
Upper Face ◽  
E1a Gene ◽  
Type Strains ◽  
Wd40 Repeats

Abstract Vegetative incompatibility, which is very common in filamentous fungi, prevents a viable heterokaryotic cell from being formed by the fusion of filaments from two different wild-type strains. Such incompatibility is always the consequence of at least one genetic difference in specific genes (het genes). In Podospora anserina, alleles of the het-e and het-d loci control heterokaryon viability through genetic interactions with alleles of the unlinked het-c locus. The het-d2Y gene was isolated and shown to have strong similarity with the previously described het-e1A gene. Like the HET-E protein, the HET-D putative protein displayed a GTP-binding domain and seemed to require a minimal number of 11 WD40 repeats to be active in incompatibility. Apart from incompatibility specificity, no other function could be identified by disrupting the het-d gene. Sequence comparison of different het-e alleles suggested that het-e specificity is determined by the sequence of the WD40 repeat domain. In particular, the amino acids present on the upper face of the predicted β-propeller structure defined by this domain may confer the incompatible interaction specificity.

scholarly journals Mutations of folC cause increased susceptibility to sulfamethoxazole in Mycobacterium tuberculosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ruiqi Wang ◽  
Kun Li ◽  
Jifang Yu ◽  
Jiaoyu Deng ◽  
Yaokai Chen
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Type Strain ◽  
Wild Type Strain ◽  
Clinical Isolates ◽  
Aminobenzoic Acid ◽  
Wild Type ◽  
Dihydropteroate Synthase ◽  
Expression Levels ◽  
Encoding Gene ◽  
Increased Susceptibility

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.

scholarly journals Isolation of a gene required for programmed initiation of development by Aspergillus nidulans.

1992 ◽  
Vol 12 (9) ◽  
pp. 3827-3833 ◽  
Author(s):  
T H Adams ◽  
W A Hide ◽  
L N Yager ◽  
B N Lee
Keyword(s):  
Life Cycle ◽  
Aspergillus Nidulans ◽  
Optimal Growth ◽  
Growth Conditions ◽  
Nutrient Deprivation ◽  
Deletion Mutants ◽  
Wild Type ◽  
Microbial Development ◽  
Type Strains ◽  
Posttranscriptional Level

In contrast to many other cases in microbial development, Aspergillus nidulans conidiophore production initiates primarily as a programmed part of the life cycle rather than as a response to nutrient deprivation. Mutations in the acoD locus result in "fluffy" colonies that appear to grow faster than the wild type and proliferate as undifferentiated masses of vegetative cells. We show that unlike wild-type strains, acoD deletion mutants are unable to make conidiophores under optimal growth conditions but can be induced to conidiate when growth is nutritionally limited. The requirement for acoD in conidiophore development occurs prior to activation of brlA, a primary regulator of development. The acoD transcript is present both in vegetative hyphae prior to developmental induction and in developing cultures. However, the effects of acoD mutations are detectable only after developmental induction. We propose that acoD activity is primarily controlled at the posttranscriptional level and that it is required to direct developmentally specific changes that bring about growth inhibition and activation of brlA expression to result in conidiophore development.

scholarly journals Influences of Histone Stoichiometry on the Target Site Preference of Retrotransposons Ty1 and Ty2 in Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 142 (3) ◽  
pp. 761-776 ◽  
Author(s):  
Lori A Rinckel ◽  
David J Garfinkel
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Promoter Region ◽  
Target Site ◽  
Site Preference ◽  
Wild Type ◽  
Histone Proteins ◽  
Protein Levels ◽  
In The Wild ◽  
Type Strains ◽  
Orientation Bias

Abstract In Saccharomyces cerevisiae, the target site specificity of the retrotransposon Ty1 appears to involve the Ty integration complex recognizing chromatin structures. To determine whether changes in chromatin structure affect Ty1 and Ty2 target site preference, we analyzed Ty transposition at the CAN1 locus in mutants containing altered levels of histone proteins. A Δhta1-htb1 mutant with decreased levels of H2A and H2B histone proteins showed a pattern of Ty1 and Ty2 insertions at CAN1 that was significantly different from that of both the wild-type and a Δhta2-htb2 mutant, which does not have altered histone protein levels. Altered levels of H2A and H2B proteins disrupted a dramatic orientation bias in the CAN1 promoter region. In the wild-type strains, few Ty1 and Ty2 insertions in the promoter region were oriented opposite to the direction of CAN1 transcription. In the Δhta1-htb1 background, however, numerous Ty1 and Ty2 insertions were in the opposite orientation clustered within the TATA region. This altered insertion pattern does not appear to be due to a bias caused by selecting canavanine resistant isolates in the different HTA1-HTB1 backgrounds. Our results suggest that reduced levels of histone proteins alter Ty target site preference and disrupt an asymmetric Ty insertion pattern.

Development of mutants of Gliocladium virens tolerant to benomyl

1990 ◽  
Vol 36 (7) ◽  
pp. 484-489 ◽  
Author(s):  
G. C. Papavizas ◽  
D. P. Roberts ◽  
K. K. Kim
Keyword(s):  
Carbon Source ◽  
Type Strain ◽  
Wild Type Strain ◽  
Carbon Sources ◽  
Sclerotium Rolfsii ◽  
Wild Type ◽  
Gliocladium Virens ◽  
Rhizosphere Competence ◽  
Filter Paper Cellulase ◽  
Type Strains

Aqueous suspensions of conidia of Gliocladium virens strains Gl-3 and Gl-21 were exposed to both ultraviolet radiation and ethyl methanesulfonate. Two mutants of Gl-3 and three of Gl-21 were selected for tolerance to benomyl at 10 μg∙mL−1, as indicated by growth and conidial germination on benomyl-amended potato dextrose agar. The mutants differed considerably from their respective wild-type strains in appearance, growth habit, sporulation, carbon-source utilization, and enzyme activity profiles. Of 10 carbon sources tested, cellobiose, xylose, and xylan were the best for growth, galactose and glucose were intermediate, and arabinose, ribose, and rhamnose were poor sources of carbon. The wild-type strains and the mutants did not utilize cellulose as the sole carbon source for growth. Two benomyl-tolerant mutants of Gl-3 produced less cellulase (β-1,4-glucosidase, carboxymethylcellulase, filter-paper cellulase) than Gl-3. In contrast, mutants of Gl-21 produced more cellulase than the wild-type strain. Only Gl-3 provided control of blight on snapbean caused by Sclerotium rolfsii. Wild-type strain Gl-21 and all mutants from both strains were ineffective biocontrol agents. Key words: Gliocladium, benomyl tolerance, Sclerotium, rhizosphere competence.

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