WITHDRAWN: Characterization of the supercomplex formed by the alternative complex III and the terminal aa oxidase from Flavobacterium johnsoniae isolated in styrene:maleic acid copolymer nanodiscs

Author(s):  
Padmaja Venkatakrishnan ◽  
Samir Benlekbir ◽  
Chang Sun ◽  
Sangjin Hong ◽  
Jonathan Hosler ◽  
...  
Author(s):  
Katarzyna Lorencik ◽  
Robert Ekiert ◽  
Yongtao Zhu ◽  
Mark J. McBride ◽  
Robert B. Gennis ◽  
...  

Energy conversion is a fundamental process of all organisms, realized by specialized protein complexes, one of which is alternative complex III (ACIII). ACIII is a functional analogue of well-known mitochondrial complex III, but operates according to a different, still unknown mechanism.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Robert Gennis ◽  
Chang Sun ◽  
Samir Benlekbir ◽  
Padmaja Venkatakrishnan ◽  
Yuhang Wang ◽  
...  

2018 ◽  
Vol 114 (3) ◽  
pp. 43a ◽  
Author(s):  
Chang Sun ◽  
Padmaja Venkatakrishnan ◽  
Samir Benlekbir ◽  
Yuhang Wang ◽  
John Rubinstein ◽  
...  

2018 ◽  
Vol 1859 ◽  
pp. e66
Author(s):  
Filipa Calisto ◽  
Joana S. Sousa ◽  
Deryck J. Mills ◽  
Julian D. Langer ◽  
Patrícia N. Refojo ◽  
...  

1978 ◽  
Vol 253 (7) ◽  
pp. 2392-2399 ◽  
Author(s):  
J.N. Siedow ◽  
S. Power ◽  
F.F. de la Rosa ◽  
G. Palmer

2001 ◽  
Vol 183 (14) ◽  
pp. 4167-4175 ◽  
Author(s):  
David W. Hunnicutt ◽  
Mark J. McBride

ABSTRACT Cells of Flavobacterium johnsoniae move over surfaces by a process known as gliding motility. The mechanism of this form of motility is not known. Cells of F. johnsoniaepropel latex spheres along their surfaces, which is thought to be a manifestation of the motility machinery. Three of the genes that are required for F. johnsoniae gliding motility,gldA, gldB, and ftsX, have recently been described. Tn4351 mutagenesis was used to identify another gene, gldD, that is needed for gliding. Tn4351-induced gldD mutants formed nonspreading colonies, and cells failed to glide. They also lacked the ability to propel latex spheres and were resistant to bacteriophages that infect wild-type cells. Introduction of wild-type gldD into the mutants restored motility, ability to propel latex spheres, and sensitivity to bacteriophage infection. gldD codes for a cytoplasmic membrane protein that does not exhibit strong sequence similarity to proteins of known function. gldE, which lies immediately upstream ofgldD, encodes another cytoplasmic membrane protein that may be involved in gliding motility. Overexpression ofgldE partially suppressed the motility defects of agldB point mutant, suggesting that GldB and GldE may interact. GldE exhibits sequence similarity to Borrelia burgdorferi TlyC and Salmonella enterica serovar Typhimurium CorC.


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