ving later, the brown rot fungi have exploited
an environmental niche relative rapidly, and
the vast majority of softwoods in the world are
degraded by brown rots. This suggests that
shifting to a LMW degradative system, with a
smaller complement of CAZymes, provides an
evolutionary advantage to the brown rots. As
discussed by Eastwood (Eastwood 2014): “The
brown rot mechanism [. . .] has evolved from a
white rot ancestry at least 5 times. This suggests
that there is a strong selection pressure for ability to cast off the energetically expensive need to
depolymerize lignin in conifer-dominated habitats.”
1. Non-enzymatic Mechanisms of Brown Rot
Fungal Wood Decay
As noted previously, brown rot fungi lack the
full complement of CAZymes and oxidoreductases necessary to deconstruct cellulose. Early
researchers studying fungal attack of wood
recognized the dilemma of having a class of
fungi that aggressively decomposed wood, but
did not have the biochemical machinery known
to be required at the time for this degradation.
In the 1960s, Cowling (Cowling 1964; Pettersson et al. 1963; Cowling 1961) noted that “readily diffusible enzyme systems” must be
responsible for the rapid depolymerization of
cellulose in brown rots, but 40 years later Cowling expressed regret for describing the active
component as a very small cellulase rather than
a LMW catalytic compound of a more general
type (personal communication). Highley, and
also Nicholas and their coworkers in the 1980s
and 1990s, noted that brown rot decay resembled wood that was treated with Fenton reagent
(Fe
2+ + H 2 O 2 ! Fe
3+ +
l OH + OH
À
); however,
results using Fenton treatment of wood alone,
or Fenton treatment with cellulolytic enzymes,
were not able to fully mimic the action of brown
rot (Highley and Illman 1991; Schmidt et al.
1981; Jin et al. 1990a; Parra et al. 1998). The
excellent research of these early researchers
demonstrated that Fenton chemistry alone was
not responsible for brown rot degradation and
that the non-enzymatic mechanism in brown
rot was more complex. Some research on
brown rot has ignored this early research, with
non-enzymatic brown rot mechanisms being
described as simple “Fenton” chemistry,
which does not reflect the complexity of the
chelator-mediated mechanism.
Research in the 1990s explored the role of
cellobiose dehydrogenase, with the finding that
this enzyme may play a role in iron reduction
and subsequent generation of hydroxyl radicals; however, this work has been discounted
because of the limited number (one) of brown
rot species found to produce cellobiose dehydrogenase. Instead, there are currently two viable working theories that describe how a LMW
catalytic system functions in brown rot fungi to
solubilize wood cell wall components in
advance of fungal enzymatic action occurring
in the wood cell lumen:
(i) The laboratory of Tanaka and Enoki has
posited that pyridine coenzymes provide
electrons to LMW glycopeptides which
can then penetrate the wood cell wall to
generate hydroxyl radicals (Kido et al.
2015). It remains unclear whether the
reductants required for the glycopeptide
systems persist in extracellular environments, and it must also be explored
whether it is feasible for glycopeptides
to diffuse into the wood cell wall to
reduce iron and then diffuse back out to
the coenzyme surrounding the fungal
hyphae to complete the redox cycle.
Because enzymes are too large to penetrate intact secondary wood cell walls,
pyridine coenzymes and other enzymes
would also not be able to penetrate, at
least until advanced stages of decay
when cell wall porosity is increased. Further, as noted by Hatakka and Hammell
(Hatakka and Hammel 2011) in discussing research with glycopeptides isolated
from a white rot fungus (Tanaka et al.
2007): “the inferred molecular masses of
the encoded peptides are around 14 kDa,
much larger than reported for the substances that were first isolated from colonized wood.” Still, genomic analysis has
found comparatively high levels of genes
encoding for Fe
3+ -reducing glycopep376
B. Goodell
an environmental niche relative rapidly, and
the vast majority of softwoods in the world are
degraded by brown rots. This suggests that
shifting to a LMW degradative system, with a
smaller complement of CAZymes, provides an
evolutionary advantage to the brown rots. As
discussed by Eastwood (Eastwood 2014): “The
brown rot mechanism [. . .] has evolved from a
white rot ancestry at least 5 times. This suggests
that there is a strong selection pressure for ability to cast off the energetically expensive need to
depolymerize lignin in conifer-dominated habitats.”
1. Non-enzymatic Mechanisms of Brown Rot
Fungal Wood Decay
As noted previously, brown rot fungi lack the
full complement of CAZymes and oxidoreductases necessary to deconstruct cellulose. Early
researchers studying fungal attack of wood
recognized the dilemma of having a class of
fungi that aggressively decomposed wood, but
did not have the biochemical machinery known
to be required at the time for this degradation.
In the 1960s, Cowling (Cowling 1964; Pettersson et al. 1963; Cowling 1961) noted that “readily diffusible enzyme systems” must be
responsible for the rapid depolymerization of
cellulose in brown rots, but 40 years later Cowling expressed regret for describing the active
component as a very small cellulase rather than
a LMW catalytic compound of a more general
type (personal communication). Highley, and
also Nicholas and their coworkers in the 1980s
and 1990s, noted that brown rot decay resembled wood that was treated with Fenton reagent
(Fe
2+ + H 2 O 2 ! Fe
3+ +
l OH + OH
À
); however,
results using Fenton treatment of wood alone,
or Fenton treatment with cellulolytic enzymes,
were not able to fully mimic the action of brown
rot (Highley and Illman 1991; Schmidt et al.
1981; Jin et al. 1990a; Parra et al. 1998). The
excellent research of these early researchers
demonstrated that Fenton chemistry alone was
not responsible for brown rot degradation and
that the non-enzymatic mechanism in brown
rot was more complex. Some research on
brown rot has ignored this early research, with
non-enzymatic brown rot mechanisms being
described as simple “Fenton” chemistry,
which does not reflect the complexity of the
chelator-mediated mechanism.
Research in the 1990s explored the role of
cellobiose dehydrogenase, with the finding that
this enzyme may play a role in iron reduction
and subsequent generation of hydroxyl radicals; however, this work has been discounted
because of the limited number (one) of brown
rot species found to produce cellobiose dehydrogenase. Instead, there are currently two viable working theories that describe how a LMW
catalytic system functions in brown rot fungi to
solubilize wood cell wall components in
advance of fungal enzymatic action occurring
in the wood cell lumen:
(i) The laboratory of Tanaka and Enoki has
posited that pyridine coenzymes provide
electrons to LMW glycopeptides which
can then penetrate the wood cell wall to
generate hydroxyl radicals (Kido et al.
2015). It remains unclear whether the
reductants required for the glycopeptide
systems persist in extracellular environments, and it must also be explored
whether it is feasible for glycopeptides
to diffuse into the wood cell wall to
reduce iron and then diffuse back out to
the coenzyme surrounding the fungal
hyphae to complete the redox cycle.
Because enzymes are too large to penetrate intact secondary wood cell walls,
pyridine coenzymes and other enzymes
would also not be able to penetrate, at
least until advanced stages of decay
when cell wall porosity is increased. Further, as noted by Hatakka and Hammell
(Hatakka and Hammel 2011) in discussing research with glycopeptides isolated
from a white rot fungus (Tanaka et al.
2007): “the inferred molecular masses of
the encoded peptides are around 14 kDa,
much larger than reported for the substances that were first isolated from colonized wood.” Still, genomic analysis has
found comparatively high levels of genes
encoding for Fe
3+ -reducing glycopep376
B. Goodell