Growth, Differentiation and Sexuality

9 Programmed Cell Death in Fungi
B.C.K. Lu 1
CONTENTS
I. Introduction ......................... 167
II. Do Fungi Have Apoptosis, the Type I
Programmed Cell Death? ................ 168
A. Apoptosis Is Induced by Expression
of Heterologous Proapoptotic Genes . . . . 168
B. Apoptosis Is Induced
byEnvironmentalStimuli ............ 169
C. Apoptosis Is Induced by Genetic Defects . 169
D. Cytological Phenotypes of Apoptosis . . . . 170
E. Caspase-LikeProteinsFound.......... 170
F. OtherRegulatorsofApoptosis......... 171
III. Heterokaryon Incompatibility ........... 172
IV. Ubiquitin-Proteasome System
and Apoptosis ........................ 172
V. Mitochondria, Oxidative Stress,
andRegulationofApoptosis............. 173
A. Role of Mitochondria in Apoptosis . . . . . 173
B. OxidativeStressinApoptosis.......... 174
C. Mitochondrial Respiration in Apoptosis . 175
D. Cytochrome c Release
and Transmembrane Potentials
inApoptosis....................... 176
E. Mitochondrial Fission and Apoptosis . . . 177
VI. AutophagyandtheTypeII
Programmed Cell Death ................ 178
A. Autophagy Is a Cellular Recycling
Program.......................... 178
B. AutophagicCellDeath(ACD) ......... 179
C. CytologicalPhenotypeofACD......... 179
D. Autophagic Cell Death
andTissueRemodeling .............. 180
VII. Meiotic Apoptosis ..................... 180
VIII. Conclusion ........................... 182
References ........................... 182
I. Introduction
Cell death may be classified into three main categories:
autophagy, apoptosis, and necrosis. The
first two are programmed and are genetically regulated,
and the third is environmentally induced
by physical or chemical injuries. Programmed cell
death (PCD) was first described in multicellular
1 Department of Molecular and Cellular Biology, University of
Guelph, Guelph, N1G 2W1 Ontario, Canada
metazoans as a developmental strategy whereby
unwanted cells are removed to make way for new
cellular remodeling and differentiation. PCD is also
essential for the removal of diseased or physiologically
and genetically defective cells (reviewed in
Ellis et al. 1991; Jacobson et al. 1997; King and Cidlowski
1998; Vaux and Korsmeyer 1999; Ranganath
and Nagashree 2001).
The type I programmed cell death or apoptosis
has been extensively studied initially in metazoans
(reviewed in Kerr et al. 1972; Wyllie et al.
1980) and now in all organisms, such as Caenorhabditis
elegans, Drosophila melanogaster, mammals,
plants and even yeasts and mycelial fungi (Hengartner
1997; Metzstein et al. 1998; Matsuyama
et al. 1999; Ranganath and Nagashree 2001). It may
be a caspase-dependent or -independent process,
and its cytological hallmarks are well defined. The
type II or autophagic cell death (ACD) is not as well
defined; it is a lysosome-dependent and a caspaseindependent
process, and it involves autophagy,
vacuolization, and cell lysis (Bursch 2001).
Research on PCD in fungi is quite recent. However,
cell death due to heterogenic incompatibility
has been documented earlier on in Podospora
anserina (Rizet and Esser 1953), Neurospora crassa
(Garnjobst and Wilson 1956; Perkins 1988), and
other filamentous fungi (see review in Esser and
Blaich 1973; Glass et al. 2000). For further reviews,
see Chap. 8 by Esser, and Chap. 7 by Glass and
Fleißner (this volume). Cell aging and senescence
have also been documented in P. anserina (Rizet
1953; Esser and Keller 1976; reviewed in Esser and
Tudzynski 1980) and other fungi (reviewed in Griffiths
1992; Osiewacz 1995; see also Hamann and
Osiewacz, Chap. 10, this volume). Senescence is
a progressive loss of growth. Visible symptoms are
hyphal tip swelling and bursting associated with
dark pigmentation that is expressed only shortly
before death. At the molecular level in P. anserina,
senescence is associated with a large number of
circular plDNA that are spliced off from mtDNA
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