| Primary Identifier | IPR035382 | Type | Family |
| Short Name | MFA1 |
| description | Many pathogenic fungi undergo morphological changes in order to infect their hosts. The Ustilago maydis pathogenic cycle starts when two mating compatible haploid yeast cells recognize each other via a pheromone-receptor system which is encoded by two sets of genes a and b []. The a locus (a1 and a2) controls the cell fusion by encoding intercellular recognition system consisting of precursors (mfa1 and mfa2) and receptors (pra1 and pra2) of lipopeptide pheromones []. The open reading frame codes for a 42-amino acid precursor, which is processed to a shorter peptide of 13 amino acids. The terminal CAAX motif is typical of farnesylated fungal pheromones, in which the last three amino acids are removed during farnesylation of the cysteine residue. This terminal cysteine is known to be O-methylated in several fungal pheromones []. Mating leads to the formation of a dikaryon filament, whose apical tip differentiates into a specialized structure for plant penetration known as the appressorium. Once inside the plant, U. maydis proliferates, inducing the formation of tumours and eventually develops into diploid spores []. This mating process requires cross-talk between cAMP and mitogen-activated protein kinase (MAPK) signaling []. Upstream regulation of a locus has been demonstrated where Hos2 (Histone deacetylases (HDACs) plant homologue) directly regulates the expression of U. maydis mating-type genes downstream of the cAMP-PKA pathway []. Furthermore, pheromone recognition blocks cell cycle progression in U. maydis cells in order to prepare mating partners for conjugation where cells undergo arrest in G2 phase [].This family includes Mfa1 proteins from Ustilgo maydis and U. hordei. |
