Emergence of Single Point Mutation in PvCesA3, Conferring Resistance to CAA Fungicides, in Plasmopara viticola Populations in Japan

2013 ◽  
Vol 14 (1) ◽  
pp. 51 ◽  
Author(s):  
Yoshinao Aoki ◽  
Maki Hashimoto ◽  
Shunji Suzuki
Keyword(s):  
Point Mutation ◽  
Single Point ◽  
Plasmopara Viticola ◽  
Single Point Mutation ◽  
Caa Fungicides ◽  
Near Future

As far as we know, there is no report of fungicide-resistant Plasmopara viticola in Japan. In the present study, we detected a single point mutation in the PvCesA3 of P. viticola sampled from a Japanese vineyard, which conferred resistance to mandipropamid. The emergence of the mandipropamid-resistant PvCesA3 allele may lead to the spread of mandipropamid-resistant P. viticola in vineyards all over Japan in the near future. Accepted for publication 23 April 2012. Published 29 July 2013.

scholarly journals Monitoring of a Single Point Mutation in the PvCesA3 Allele Conferring Resistance to Carboxylic Acid Amide Fungicides in Plasmopara viticola Populations In Yamanashi Prefecture, Japan

2015 ◽  
Vol 16 (2) ◽  
pp. 84-87 ◽  
Author(s):  
Yoshinao Aoki ◽  
Yumi Kawagoe ◽  
Nozomi Fujimori ◽  
Sayumi Tanaka ◽  
Shunji Suzuki
Keyword(s):  
Carboxylic Acid ◽  
Point Mutation ◽  
Fungicide Resistance ◽  
Single Point ◽  
Acid Amide ◽  
Plasmopara Viticola ◽  
Single Point Mutation ◽  
Carboxylic Acid Amide ◽  
Grapevine Downy Mildew ◽  
Quinone Outside Inhibitor

The use of the carboxylic acid amide (CAA) fungicide mandipropamid to manage grapevine downy mildew in vineyards in Japan has been increasing since 2010, because of widespread quinone outside inhibitor fungicide resistance in the Plasmopara viticola population. However, CAA fungicide resistance in P. viticola is becoming a serious problem worldwide. In 2013, we monitored for the presence of a single point mutation at codon 1105 of the cellulose synthase gene PvCesA3, which confers resistance to mandipropamid in P. viticola samples collected from four vineyards in Yamanashi prefecture in Japan. Five out of 157 samples were found to be heterozygotes, carrying both the mutated and nonmutated PvCesA3 alleles. Although CAA fungicide-resistant P. viticola isolates have not been reported yet in Japan, the emergence of heterozygous P. viticola populations indicates the potential risk of emergence of resistant homozygotes. Accepted for publication 14 March 2015. Published 1 May 2015

scholarly journals A single point mutation converts a proton-pumping rhodopsin into a red-shifted, turn-on fluorescent sensor for chloride

2021 ◽  
Author(s):  
Jasmine N. Tutol ◽  
Jessica Lee ◽  
Hsichuan Chi ◽  
Farah N. Faizuddin ◽  
Sameera S. Abeyrathna ◽  
...  
Keyword(s):  
Point Mutation ◽  
Fluorescent Sensor ◽  
Single Point ◽  
Proton Pumping ◽  
Single Point Mutation ◽  
Turn On ◽  
Gloeobacter Violaceus

By utilizing laboratory-guided evolution, we have converted the fluorescent proton-pumping rhodopsin GR from Gloeobacter violaceus into GR1, a red-shifted, turn-on fluorescent sensor for chloride.

scholarly journals Structural basis for a complex I mutation that blocks pathological ROS production

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhan Yin ◽  
Nils Burger ◽  
Duvaraka Kula-Alwar ◽  
Dunja Aksentijević ◽  
Hannah R. Bridges ◽  
...  
Keyword(s):  
Point Mutation ◽  
Complex I ◽  
Structural Changes ◽  
Ischemia Reperfusion ◽  
Single Point ◽  
Structural Basis ◽  
Single Point Mutation ◽  
Ros Production

AbstractMitochondrial complex I is central to the pathological reactive oxygen species (ROS) production that underlies cardiac ischemia–reperfusion (IR) injury. ND6-P25L mice are homoplasmic for a disease-causing mtDNA point mutation encoding the P25L substitution in the ND6 subunit of complex I. The cryo-EM structure of ND6-P25L complex I revealed subtle structural changes that facilitate rapid conversion to the “deactive” state, usually formed only after prolonged inactivity. Despite its tendency to adopt the “deactive” state, the mutant complex is fully active for NADH oxidation, but cannot generate ROS by reverse electron transfer (RET). ND6-P25L mitochondria function normally, except for their lack of RET ROS production, and ND6-P25L mice are protected against cardiac IR injury in vivo. Thus, this single point mutation in complex I, which does not affect oxidative phosphorylation but renders the complex unable to catalyse RET, demonstrates the pathological role of ROS production by RET during IR injury.

Scarcity of λ1 B cells in mice with a single point mutation in Cλ1 is due to a low BCR signal caused by misfolded lambda1 light chain

2007 ◽  
Vol 44 (6) ◽  
pp. 1417-1428 ◽  
Author(s):  
Veronica V. Volgina ◽  
Tianhe Sun ◽  
Grazyna Bozek ◽  
Terence E. Martin ◽  
Ursula Storb
Keyword(s):  
B Cells ◽  
Point Mutation ◽  
Light Chain ◽  
Single Point ◽  
Single Point Mutation

Shifting Substrate Specificity of Human Glutathione Transferase (from Class Pi to Class Alpha) by a Single Point Mutation

1998 ◽  
Vol 252 (1) ◽  
pp. 184-189 ◽  
Author(s):  
Marzia Nuccetelli ◽  
Anna P. Mazzetti ◽  
Jamie Rossjohn ◽  
Michael W. Parker ◽  
Philip Board ◽  
...  
Keyword(s):  
Substrate Specificity ◽  
Point Mutation ◽  
Glutathione Transferase ◽  
Single Point ◽  
Single Point Mutation
Sign in / Sign up

Export Citation Format

Share Document