The ukb1 gene encodes a putative protein kinase required for bud
site selection and pathogenicity in Ustilago maydis
G. Yang, and J.W. Kronstad
Biotechnology Laboratory, Department of Microbiology and Immunology, Faculty of Agricultural Sciences, University of British Columbia,
237-6174 University Blvd., Vancouver, BC, Canada V6T 1Z3
Received 28 February 2002; accepted 29 April 2002
Morphogenesis and pathogenesis are closely associated aspects of the life cycle of the fungal pathogen Ustilago maydis. In this
fungus, the dimorphic switch from budding to ﬁlamentous growth coincides with the transition from non-pathogenic to pathogenic
growth on maize. We have cloned and characterized the ukb1 gene that encodes a putative serine/threonine protein kinase with a role
in budding and ﬁlamentous growth. Mutants defective in ukb1 were altered in bud site selection and produced lateral buds at a
greater frequency than wild-type cells. Dikaryotic cells defective in ukb1 were capable of colonizing host tissue and growing with a
ﬁlamentous morphology in planta. However, the mutants were incapable of inducing tumor formation and they failed to complete
sexual development. In addition, the ukb1 gene inﬂuenced the ability of colonies to form aerial mycelia in response to environmental
stimuli. Overall, the discovery of ukb1 reinforces the connection between morphogenesis and pathogenesis in U. maydis.
Ó 2002 Elsevier Science (USA). All rights reserved.
Keywords: Signaling; Bud site selection; Tumorigenesis; Protein kinase
The ability to switch from budding to ﬁlamentous
growth is a key aspect of the Ustilago maydis life cycle
(reviewed in Banuett, 1995). U. maydis haploid sporidia
are non-pathogenic and have a budding morphology.
Upon mating, compatible sporidia can fuse and subse-
quently diﬀerentiate into an infectious ﬁlamentous di-
karyon. This change from budding to ﬁlamentous
growth coincides with a change of lifestyle from sapro-
phytic to pathogenic development. The infectious hy-
phae colonize maize tissue and induce the formation of
tumors. Dikaryotic cells undergo karyogamy inside the
tumor tissue and the resulting diploid cells diﬀerentiate
into highly melanized teliospores. Tremendous masses
of black teliospores accumulate in the tumors and the
tissue eventually bursts to disperse the spores for sub-
sequent inoculation of other plants. Under appropriate
conditions, the teliospores germinate and undergo mei-
osis to generate haploid sporidia.
The transition from saprophytic budding growth to
pathogenic ﬁlamentous growth is initiated upon suc-
cessful mating. Mating in U. maydis is governed by a
tetrapolar mating system with two loci called a and b:
the a locus has two speciﬁcities (a1 and a2) and the b
locus has at least 25 naturally occurring speciﬁcities
(reviewed in Kronstad and Staben, 1997). The fusion of
mating-compatible haploid cells is governed by the a
locus, which encodes a two component pheromone sig-
naling system composed of a pheromone peptide and a
pheromone receptor (B
oolker et al., 1992). Receptor
binding of pheromone triggers the formation of a con-
jugation tube, enabling cell fusion and subsequent
interaction of the products of the b locus. The b locus has
two divergently transcribed genes designated bE and bW
(Gillissen et al., 1992; Kronstad and Leong, 1989, 1990;
Schulz et al., 1990). The bE and bW proteins contain
homeodomains and these protein are known to dimerize
if they are of diﬀerent speciﬁcities (K
aamper et al., 1995).
Fungal Genetics and Biology 37 (2002) 98–108
This paper is dedicated to the memory of Ge Yang, a talented
scientist who tragically died during the course of this work.
Corresponding author. Fax: +604-822-6097.
E-mail address: firstname.lastname@example.org (J.W. Kronstad).
Present address: Department of Plant Pathology, Cornell Univer-
sity, Ithaca, New York.
1087-1845/02/$ - see front matter Ó 2002 Elsevier Science (USA). All rights reserved.
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