Ustilago maydis, a fungal pathogen of maize, alternates between budding and filamentous growth in response to mating and other environmental signals. Defects in components of the cAMP signaling pathway affect this morphological transition and reveal an association of budding growth with elevated cAMP levels and filamentous growth with low cAMP levels. We have identified two genes, adr1 and uka1, encoding catalytic subunits of cAMP-dependent protein kinase (PKA). Disruption of adr1 resulted in a constitutively filamentous growth phenotype similar to that of mutants deficient in adenylyl cyclase. Importantly, adr1 is required for pathogenicity and is responsible for the majority of PKA activity in fungal cells. In contrast, uka1 has little inf luence on pathogenicity, and deletion of the uka1 gene does not affect cell morphology. These results provide compelling evidence that regulated PKA activity is crucial during infectious development of U. maydis.Pathogenesis, dimorphic growth, and sexual development are intricately interconnected in the corn smut fungus Ustilago maydis, and the perception of signals from the host plant is likely to play an important role in these processes (1, 2). Mating of haploid U. maydis cells, which are nonpathogenic and yeast-like, leads to the formation of infectious, dikaryotic hyphae. Dikaryons can be established in culture, but the resulting hyphae need the host environment to sustain mycelial proliferation. Infection of maize plants results in tumor induction and the eventual formation of masses of diploid teliospores.
The fungal pathogen Ustilago hordei causes the covered smut disease of barley and oats. Mating and pathogenicity in this fungus are controlled by the MAT locus, which contains two distinct gene complexes, a and b. In this study, we tagged the a and b regions with the recognition sequence for the restriction enzyme I-SceI and determined that the distance between the complexes is 500 kb in a MAT-1 strain and 430 kb in a MAT-2 strain. Characterization of the organization of the known genes within the a and b gene complexes provided evidence for nonhomology and sequence inversion between MAT-1 and MAT-2. Antibiotic-resistance markers also were used to tag the a gene complex in MAT-1 strains (phleomycin) and the b gene complex in MAT-2 strains (hygromycin). Crosses were performed with these strains and progeny resistant to both antibiotics were recovered at a very low frequency, suggesting that recombination is suppressed within the MAT region. Overall, the chromosome homologues carrying the MAT locus of U. hordei share features with primitive sex chromosomes, with the added twist that the MAT locus also controls pathogenicity.MAT locus ͉ sex chromosome ͉ smut disease ͉ phytopathogen ͉ basidiomycete U stilago hordei represents a group of fungal pathogens that cause economically important smut diseases on small-grain cereals (1). These fungi grow as hyphae within developing seedlings without causing symptoms; upon flowering of the host plant, the fungal cells proliferate and form masses of dark teliospores that replace the seeds. The diploid teliospores germinate and undergo meiosis to yield haploid cells. These meiotic progeny must mate to infect the host, and infection is a prerequisite for completion of the sexual phase of the life cycle, i.e., the formation of teliospores. Sex and pathogenicity therefore are interconnected in U. hordei and related smut fungi, and the mating-type genes are considered pathogenicity factors.U. hordei has a bipolar mating system controlled by one mating-type locus (MAT) with two alleles or alternative specificities, MAT-1 and MAT-2. DNA hybridization experiments with the well-characterized a and b mating-type genes from the related species, Ustilago maydis, revealed that U. hordei possesses similar mating-type functions located at so-called a and b gene complexes within the MAT locus (2, 3). In contrast to U. hordei, U. maydis has a tetrapolar mating system because the a and b loci are on separate chromosomes and therefore segregate independently during meiosis (3, 4). Thus, the tetrapolar and bipolar mating systems are distinguished by differences in the genomic organizations of the a and b genes (3). In U. maydis, two specificities exist for the a locus: a1 and a2 (5, 6). The a locus encodes cell-type specific pheromones (mfa) as well as the pheromone receptors (pra) that recognize pheromones from compatible mating partners. The b locus of U. maydis is multiallelic and contains two divergently transcribed genes, bE (bEast) and bW (bWest) (4, 7-9). The b locus controls pathogenicity ...
To investigate the effects of bilateral intrathoracic vagotomy on the establishment of continuous breathing and effective gas exchange at birth, we studied 8 chronically instrumented, unanesthetized, sham-operated and 14 vagotomized newborn lambs after a spontaneous, unassisted vaginal delivery. Fetal lambs were instrumented in utero to record sleep states, diaphragmatic electromyogram, blood pressure, arterial pH, and blood-gas tensions. Six of eight sham-operated lambs established effective gas exchange within 10 min of birth, whereas 12 of 14 vagotomized animals developed respiratory acidosis and hypoxemia (P = 0.008). Breathing frequency in vagotomized newborns was significantly lower during the entire postnatal period compared with sham-operated newborns. Vagotomized subjects also remained hypothermic during the entire postnatal period (P < 0.05). Bronchoalveolar lavage indicated an increased minimum surface tension, whereas lung histology showed perivascular edema and partial atelectasis in the vagotomized group. We conclude that stimulation of breathing and effective gas exchange are critically dependent on intact vagal nerves during the transition from fetal to neonatal life.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.