Growth, Differentiation and Sexuality

Loculoascomycete vs. Pyrenomycete MAT1-1 loci,
which consist of a single gene in the former, and
three genes in the latter. Perhaps the finding that
the Loculoascomycete proteins may be hybrid MAT
proteins dictates these differences (see Fig 15.5).
V. Functions of Mating-Type Genes
Very little is known about the target genes to which
the mating-type transcription factors bind while
MAT1-1-2 encodesproteinsofunknownfunctions.
Therefore, the developmental processes controlled
by the mating-type genes cannot be directly
inferred from the molecular functions of the
proteins they encode. Instead, their biological role
has been deduced from the effect of mating-type
gene mutations on the sexual cycle. These analyses
comprised qualitative and quantitative examinations
of progeny, and cytological observations of
the development inside the fruiting body. Deletion
of the MAT loci from different fungi confirmed
that they contain the essential regulatory genes
for fertilization, but ΔMAT strains still produce
pre-fertilization male and female reproductive
structures, indicating that mating types are
not involved in the developmental switch from
vegetative stage to sexual reproduction (Coppin
et al. 1993; Ferreira et al. 1998). In addition to
the role of mating types during fertilization,
genetic and cytological observations show that
they are required also during the formation of
the fruiting body. We will briefly summarize
the main conclusions about the mating-type
gene biological functions in the different model
systems.
A. Functions of Mating-Type Genes During
Fertilization
1. Regulatory Functions of Mating-Type Genes
Fertilization or mating requires a recognition step
between sexually compatible strains, leading to the
entry of a nucleus into the female organ (Fig. 15.1).
In self-incompatible species, this step occurs between
a female organ and a donor cell of opposite
mating type. Several lines of evidence demonstrate
that MAT1-1-1 and MAT1-2-1 genes are the master
genes regulating fertilization in self-incompatible
Euascomycetes. Deletion of the MAT locus in N.
crassa (Ferreira et al. 1998) or C. heterostrophus
Mating Types in Euascomycetes 315
(Wirsel et al. 1996) leads to complete absence of
mating, while P. anserina ΔMAT strains, considered
initially as completely mating deficient (Coppin
et al. 1993), in fact display a very low mating
ability (Arnaise et al. 2001). Transformation of the
ΔMAT strains with wild-type MAT1-1-1 or MAT1-
2-1 restores mating ability to a wild-type level in the
three fungi (Debuchy et al. 1993; Wirsel et al. 1996,
1998; Ferreira et al. 1998). The regions required
for fertilization in mat A-1 and mat a-1 have been
determined in detail in N. crassa. MutationA m99
was localized inside the α1 encoding region of mat
A-1, and converted the conserved tryptophan at
position 86 to a stop codon (Fig. 15.4; Saupe et al.
1996). The corresponding strain is completely male
sterile, but surprisingly still female fertile, albeit to
a reduced level. Further analyses of a series of mat
A-1 mutations indicated that mating as male requires
a complete α1 domain and residues up to
position 227. These results suggest that the target
genesrequiredforfemaleandmalefertilitymaybe
regulated differently by mat A-1, for instance, by
the interaction of mat A-1 with cofactors specific
to female and male organs. Deletion analyses of
mat a-1 indicates that an intact HMG domain and
the C-terminal tail are required for mating (Philley
and Staben 1994). The sequence within the terminal
180 amino acids required for mating does not
appear to be very specific; the P. anserina FPR1
gene confers mating in N. crassa, althoughitencodes
a carboxyl terminus quite different from that
of mat a-1 (Arnaise et al. 1993). Taken together,
these data indicate that MAT1-1-1 and MAT1-2-1
are activators of the functions required for fertilization.
Mutations in FMR1, SMR2 and FPR1 in P. anserina
revealed a more complex wiring (Arnaise et al.
2001). Mutations in FPR1 that did not affect the
mat+ mating function resulted in mat+ strains
that were capable of selfing. Consistent with the
idea that these strains became self-fertile, they produced
male cells able to fertilize a mat+ strain. This
phenotype indicates that these mutations have relieved
repression of the mat– functions required for
mating, suggesting that the wild-type FPR1 gene
represses these functions in mat+ sexual organs
(Fig. 15.9). Similarly, mutations leading to selffertilityhavebeenobservedinFMR1,
and more
surprisingly in SMR2. IncontrasttoFMR1, SMR2
is not required for the expression of mat– mating
function,butitappearsnowtobenecessarytogether
with FMR1 for the repression of mat+ fertilization
functions in mat– sexual organs (Fig. 15.9).