REN1 Is Required for Development of Microconidia and Macroconidia, but Not of Chlamydospores, in the Plant Pathogenic Fungus Fusarium oxysporum

Author:

Ohara Toshiaki1,Inoue Iori1,Namiki Fumio2,Kunoh Hitoshi3,Tsuge Takashi1

Affiliation:

1. Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan

2. National Agricultural Research Center for Kyushu-Okinawa Region, Nishigoshi-Machi, Kikuchi-Gun 861-1192, Japan

3. Faculty of Bioresources, Mie University, Tsu 514-0008, Japan

Abstract

Abstract The filamentous fungus Fusarium oxysporum is a soil-borne facultative parasite that causes economically important losses in a wide variety of crops. F. oxysporum exhibits filamentous growth on agar media and undergoes asexual development producing three kinds of spores: microconidia, macroconidia, and chlamydospores. Ellipsoidal microconidia and falcate macroconidia are formed from phialides by basipetal division; globose chlamydospores with thick walls are formed acrogenously from hyphae or by the modification of hyphal cells. Here we describe rensa, a conidiation mutant of F. oxysporum, obtained by restriction-enzyme-mediated integration mutagenesis. Molecular analysis of rensa identified the affected gene, REN1, which encodes a protein with similarity to MedA of Aspergillus nidulans and Acr1 of Magnaporthe grisea. MedA and Acr1 are presumed transcription regulators involved in conidiogenesis in these fungi. The rensa mutant and REN1-targeted strains lack normal conidiophores and phialides and form rod-shaped, conidium-like cells directly from hyphae by acropetal division. These mutants, however, exhibit normal vegetative growth and chlamydospore formation. Nuclear localization of Ren1 was verified using strains expressing the Ren1-green fluorescent protein fusions. These data strongly suggest that REN1 encodes a transcription regulator required for the correct differentiation of conidiogenesis cells for development of microconidia and macroconidia in F. oxysporum.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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