Heterotrimeric G protein β subunit GPB1 and MAP kinase MPK1 regulate hyphal growth and female fertility in Fusarium sacchari

Mycoscience ◽  
2013 ◽  
Vol 54 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Isao Kaneko ◽  
Makoto Iyama-Kadono ◽  
Kana Togashi-Nishigata ◽  
Isamu Yamaguchi ◽  
Tohru Teraoka ◽  
...  
2004 ◽  
Vol 3 (6) ◽  
pp. 1653-1663 ◽  
Author(s):  
Sherif Ganem ◽  
Shun-Wen Lu ◽  
Bee-Na Lee ◽  
David Yu-Te Chou ◽  
Ruthi Hadar ◽  
...  

ABSTRACT Previous work established that mutations in mitogen-activated protein (MAP) kinase (CHK1) and heterotrimeric G-protein α (Gα) subunit (CGA1) genes affect the development of several stages of the life cycle of the maize pathogen Cochliobolus heterostrophus. The effects of mutating a third signal transduction pathway gene, CGB1, encoding the Gβ subunit, are reported here. CGB1 is the sole Gβ subunit-encoding gene in the genome of this organism. cgb1 mutants are nearly wild type in vegetative growth rate; however, Cgb1 is required for appressorium formation, female fertility, conidiation, regulation of hyphal pigmentation, and wild-type virulence on maize. Young hyphae of cgb1 mutants grow in a straight path, in contrast to those of the wild type, which grow in a wavy pattern. Some of the phenotypes conferred by mutations in CGA1 are found in cgb1 mutants, suggesting that Cgb1 functions in a heterotrimeric G protein; however, there are also differences. In contrast to the deletion of CGA1, the loss of CGB1 is not lethal for ascospores, evidence that there is a Gβ subunit-independent signaling role for Cga1 in mating. Furthermore, not all of the phenotypes conferred by mutations in the MAP kinase CHK1 gene are found in cgb1 mutants, implying that the Gβ heterodimer is not the only conduit for signals to the MAP kinase CHK1 module. The additional phenotypes of cgb1 mutants, including severe loss of virulence on maize and of the ability to produce conidia, are consistent with CGB1 being unique in the genome. Fluorescent DNA staining showed that there is often nuclear degradation in mature hyphae of cgb1 mutants, while comparable wild-type cells have intact nuclei. These data may be genetic evidence for a novel cell death-related function of the Gβ subunit in filamentous fungi.


2020 ◽  
Vol 22 (10) ◽  
Author(s):  
Marco Iván Valle‐Maldonado ◽  
José Alberto Patiño‐Medina ◽  
Carlos Pérez‐Arques ◽  
Nancy Yadira Reyes‐Mares ◽  
Irvin Eduardo Jácome‐Galarza ◽  
...  

2000 ◽  
Vol 20 (1) ◽  
pp. 352-362 ◽  
Author(s):  
Ping Wang ◽  
John R. Perfect ◽  
Joseph Heitman

ABSTRACT Cryptococcus neoformans is an opportunistic fungal pathogen with a defined sexual cycle. The gene encoding a heterotrimeric G-protein β subunit, GPB1, was cloned and disrupted.gpb1 mutant strains are sterile, indicating a role for this gene in mating. GPB1 plays an active role in mediating responses to pheromones in early mating steps (conjugation tube formation and cell fusion) and signals via a mitogen-activated protein (MAP) kinase cascade in both MATα and MATa cells. The functions of GPB1 are distinct from those of the Gα protein GPA1, which functions in a nutrient-sensing cyclic AMP (cAMP) pathway required for mating, virulence factor induction, and virulence.gpb1 mutant strains are also defective in monokaryotic fruiting in response to nitrogen starvation. We show thatMATa cells stimulate monokaryotic fruiting ofMATα cells, possibly in response to mating pheromone, which may serve to disperse cells and spores to locate mating partners. In summary, the Gβ subunit GPB1 and the Gα subunit GPA1 function in distinct signaling pathways: one (GPB1) senses pheromones and regulates mating and haploid fruiting via a MAP kinase cascade, and the other (GPA1) senses nutrients and regulates mating, virulence factors, and pathogenicity via a cAMP cascade.


1997 ◽  
Vol 272 (30) ◽  
pp. 18801-18807 ◽  
Author(s):  
Mingyao Liu ◽  
Bo Yu ◽  
Osamu Nakanishi ◽  
Thomas Wieland ◽  
Melvin Simon

2001 ◽  
pp. 147-152
Author(s):  
Tatsuo Iwasa ◽  
Kazue Kanehara ◽  
Ayako Watari ◽  
Mahito Ohkuma ◽  
Masashi Nakagawa ◽  
...  

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