Despite the importance of cell wall diffusion to nearly all aspects of wood utilization, diffusion mechanisms and the detailed effects of moisture remain poorly understood. In this perspective, we introduce and employ approaches established in polymer science to develop a phenomenological framework for understanding the effects of moisture on diffusion in unmodified wood cell walls. The premise for applying this polymer-science-based approach to wood is that wood polymers (cellulose, hemicelluloses, and lignin) behave like typical solid polymers. Therefore, the movement of chemicals through wood cell walls is a diffusion process through a solid polymer, which is in contrast to previous assertions that transport of some chemicals occurs via aqueous pathways in the cell wall layers. Diffusion in polymers depends on the interrelations between free volume in the polymer matrix, molecular motions of the polymer, diffusant dimensions, and solubility of the diffusant in the polymer matrix. Because diffusion strongly depends on whether a polymer is in a rigid glassy state or soft rubbery state, it is important to understand glass transitions in the amorphous wood polymers. Through a review and analysis of available literature, we conclude that in wood both lignin and the amorphous polysaccharides very likely have glass transitions. After developing and presenting this polymer-science-based perspective of diffusion through unmodified wood cell walls, suggested directions for future research are discussed. A key consideration is that a large difference between diffusion through wood polymers and typical polymers is the high swelling pressures that can develop in unmodified wood cell walls. This pressure likely arises from the hierarchical structure of wood and should be taken into consideration in the development of predictive models for diffusion in unmodified wood cell walls.

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Brown rot (BR) decay mechanisms employ carbohydrate-active enzymes (CAZymes) as well as a unique non-enzymatic chelator-mediated Fenton (CMF) chemistry to deconstruct lignocellulosic materials. Unlike white rot fungi, BR fungi lack peroxidases for lignin deconstruction, and also lack some endoglucanase/cellobiohydrolase activities. The role that the CMF mechanism plays in “opening up” the wood cell wall structure in advance of enzymatic action, and any interaction between CMF constituents and the selective CAZyme suite that BRs possess, is still unclear. Expression patterns for CMF redox metabolites and lytic polysaccharide monooxygenase (LPMO–AA9 family) genes showed that some LPMO isozymes were upregulated with genes associated with CMF at early stages of brown rot by Gloeophyllum trabeum . In the structural studies, wood decayed by the G. trabeum was compared to CMF-treated wood, or CMF-treated wood followed by treatment with either the early-upregulated LPMO or a commercial CAZyme cocktail. Structural modification of decayed/treated wood was characterized using small angle neutron scattering. CMF treatment produced neutron scattering patterns similar to that of the BR decay indicating that both systems enlarged the nanopore structure of wood cell walls to permit enzyme access. Enzymatic deconstruction of cellulose or lignin in raw wood samples was not achieved via CAZyme cocktail or LPMO enzyme action alone. CMF treatment resulted in depolymerization of crystalline cellulose as attack progressed from the outer regions of individual crystallites. Multiple pulses of CMF treatment on raw wood showed a progressive increase in the spacing between the cellulose elementary fibrils (EFs), indicating the CMF eroded the matrix outside the EF bundles, leading to less tightly packed EFs. Peracetic acid delignification treatment enhanced subsequent CMF treatment effects, and allowed both enzyme systems to further increase spacing of the EFs. Moreover, even after a single pulse of CMF treatment, both enzymes were apparently able to penetrate the cell wall to further increase EF spacing. The data suggest the potential for the early-upregulated LPMO enzyme to work in association with CMF chemistry, suggesting that G. trabeum may have adopted mechanisms to integrate non-enzymatic and enzymatic chemistries together during early stages of brown rot decay.