Deletion mutations in PPH22, FAR8, and MOB3 lead to defects in sexual differentiation.

(A) PPH22/pph22Δ and MOB3/mob3Δ strains exhibit defects in self-filamentation compared to WT/WT (CnLC6683). Images were taken after four weeks of incubation on MS plates at room temperature. Scale bars represent 200 μm. (B) Mating efficiency of STRIPAK...

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التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Patricia P. Peterson (20291306) (author)
مؤلفون آخرون:	Jin-Tae Choi (17118299) (author), Ci Fu (148006) (author), Leah E. Cowen (7431083) (author), Sheng Sun (142836) (author), Yong-Sun Bahn (210099) (author), Joseph Heitman (22335) (author)
منشور في:	2024
الموضوعات:	Biochemistry Medicine Microbiology Cell Biology Genetics Evolutionary Biology Ecology Developmental Biology Infectious Diseases Virology Biological Sciences not elsewhere classified Chemical Sciences not elsewhere classified significant fitness disadvantage murine infection model heterotrimeric enzyme composed haploid background leads div >< p abnormal cell morphology >, namely pp2aa genome sequencing revealed 30 ° c regulatory b subunit protein interactions suggest protein domain analysis including impaired hyphae calcineurin inhibitors cyclosporine b ”’ subunit suggesting stripak functions severely reduced growth maintaining genome stability catalytic c subunit cryptococcus neoformans </ δ exhibit defects stripak complex plays stripak components pph22 genome stability stripak components c </ growth defects neoformans </ detected protein calcineurin activity vegetative growth hyphal growth pph22 </ ppg1 </ δ mutants type diploid taken together synthetically lethal structural modeling sexual differentiation sexual development protein striatin interacting phosphatase increased segmental important role impaired virulence haploinsufficient gene functionally characterized findings reveal eukaryotic serine elevated temperature deletion mutants chromosomal aneuploidy capsule production basidiospore production assembled similarly also unable
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Deletion mutations in <i>PPH22</i>, <i>FAR8</i>, and <i>MOB3</i> lead to defects in sexual differentiation.

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