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Compartmentalization of decay in trees

Compartmentalization of Decay in Trees (CODIT) is a natural defense mechanism and conceptual model that explains how woody plants isolate and contain injury, infection, and decay within discrete compartments of their vascular tissues, preventing widespread damage and promoting long-term survival.^[1] First proposed by plant pathologist Alex L. Shigo in the 1970s and refined through subsequent research, CODIT emphasizes that trees do not "heal" wounds like animal tissue but instead respond by reinforcing pre-existing anatomical boundaries and generating new barriers to limit the progression of pathogens and decay fungi.^[2] This process relies on the tree's highly compartmented structure, formed by living parenchyma cells that produce both physical and chemical defenses, allowing the organism to allocate resources efficiently while continuing growth around affected areas.^[1] The CODIT model delineates four principal "walls" that trees erect in response to damage, each targeting a specific direction of potential decay spread in the three-dimensional xylem network.^[2] Wall 1 forms immediately after injury to block axial (vertical) movement through vessels and tracheids, using anatomical responses like tyloses, gels, and ballooning of parenchyma cells, combined with chemical inhibitors to seal pathways upward and downward.^[1] Wall 2 resists radial (inward) spread toward the tree's core by strengthening annual growth rings, particularly through lignified latewood cells and the production of antimicrobial phenolics from axial parenchyma.^[2] Wall 3, the most robust pre-formed barrier, utilizes ray parenchyma tissues to confine tangential (lateral) progression between annual rings, leveraging their interconnected lattice for rapid signaling and metabolite transport.^[1] Wall 4, unique in being newly created post-injury, consists of a suberized and lignified barrier zone generated by the vascular cambium, which isolates decay from emerging sapwood and supports the formation of woundwood callus.^[2] These walls integrate physical compartmentalization with biochemical defenses, where parenchyma cells convert non-structural carbohydrates into secondary metabolites such as phytoanticipins (pre-formed compounds like tannins in heartwood) and phytoalexins (induced antimicrobials like flavonoids and terpenoids) to inhibit fungal and bacterial invaders.^[2] Decay typically begins with pioneer microbes entering sapwood via wounds, but effective CODIT confines it to older heartwood, minimizing impacts on hydraulic function and mechanical strength.^[1] The model's efficacy depends on factors like tree species, age, wound size, and environmental stress, with stronger responses in healthy trees boasting ample energy reserves.^[2] In arboriculture and forestry, recognizing CODIT guides practices such as proper pruning to avoid compromising barriers, reducing risks of structural failure or accelerated decay.^[1]

Theoretical Foundations

Historical Development

The understanding of decay in trees evolved significantly in the late 19th century through the pioneering work of Robert Hartig, a German forester and pathologist often regarded as the founder of forest pathology. Hartig's research focused on wood-decay fungi, demonstrating their role as active agents in breaking down tree tissues rather than mere byproducts of decomposition.^[3] In 1874, he conducted key experiments proving that specific fungi, such as those causing heart rot, initiate and drive decay processes in wounded or stressed trees.^[4] This marked a pivotal shift from the prevailing theory of spontaneous generation, which posited that decay arose abiogenetically in damaged wood, to a microbial causation model aligned with the emerging germ theory of disease. Hartig's inoculation studies refuted spontaneous generation by showing that uninfected wood remained sound unless exposed to fungal spores, establishing a causal link between microorganisms and tree decay.^[3] His 1894 book, Text-book of the Diseases of Trees (English translation of the original German Lehrbuch der Baumkrankheiten), synthesized these findings into a comprehensive foundational text, detailing fungal life cycles, infection pathways, and disease management in forest trees.^[5] Building on Hartig's microbial framework, American plant pathologist Alex L. Shigo advanced the field in the 1970s through systematic investigations into decay patterns and tree responses to injury. Shigo's research involved dissecting over 10,000 trees to map discoloration and decay columns, revealing that trees do not simply succumb passively to infection but actively limit its spread through compartmentalized barriers.^[6] These observations led to the formulation of the Compartmentalization of Decay in Trees (CODIT) model, which expanded classical decay concepts to emphasize the tree's ordered, dynamic defenses. This culminated in Shigo's influential 1979 USDA Forest Service Agriculture Information Bulletin No. 419, Tree Decay: An Expanded Concept, which formalized CODIT and integrated microbial succession with anatomical responses for practical applications in arboriculture and forestry.^[7]

Core Concepts

Trees are modular organisms characterized by a high degree of compartmentalization, consisting of numerous independent functional units that enable localized responses to damage. These units include xylem vessels for water transport, phloem sieve tubes for nutrient distribution, and ray parenchyma cells that facilitate radial movement of substances within the wood. This modular structure allows trees to function as a collection of interconnected yet semi-autonomous "sub-trees," with each annual growth ring representing a distinct layer that can operate independently from others.^[8] A fundamental distinction exists between healing and compartmentalization in tree biology. Healing refers to the regenerative process where damaged tissues are repaired or replaced in their original positions, such as through the proliferation of new cells to close a wound surface. In contrast, compartmentalization involves the isolation of injured or infected areas to prevent the spread of decay, without necessarily regenerating the lost tissue; instead, trees form boundaries that contain pathogens and limit their progression through the vascular system.^[9] Compartmentalization of decay, often abbreviated as CODIT, serves as an evolved defense strategy that protects trees from pathogens, insects, and mechanical injuries by confining defects to specific regions. This process has developed over evolutionary time to enhance survival, allowing long-lived woody perennials to persist despite repeated wounding by isolating threats and preserving vital functions in unaffected compartments. The CODIT model, synthesized by Alex Shigo based on extensive dissections of thousands of trees, encapsulates these principles as a comprehensive framework for understanding tree resilience.^[8]^[9] Central to CODIT are basic anatomical features that facilitate decay containment. Annual growth rings, formed by seasonal increments of xylem tissue, create concentric layers that act as natural boundaries between older and newer wood. The vascular cambium, a thin layer of meristematic cells between the bark and wood, generates new tissues annually and plays a key role in producing protective responses to injury. At the core, the pith structure provides the initial axis around which growth expands, influencing how decay patterns radiate or are restricted.^[10]^[9]

Mechanisms of Compartmentalization

The Four Barrier Walls

The compartmentalization of decay in trees (CODIT) model delineates four conceptual barrier walls that trees form to isolate and contain decay following wounding, directing the response along anatomical lines of weakness in wood structure. These walls operate in three dimensions—longitudinal, radial, and tangential—to limit the spread of pathogens and prevent widespread tissue degradation. Wall 1 and Wall 2 form the initial boundaries using pre-existing wood anatomy, while Wall 3 and Wall 4 develop as active responses post-injury, with their effectiveness varying by tree species, age, and wound severity. Wall 1, the longitudinal or vertical barrier, is formed by ray parenchyma cells that plug vascular tissues, such as vessels and tracheids, along the grain of the wood. This wall limits the upward and downward spread of decay by sealing conduits through tyloses, gels, or phenolic deposits produced by adjacent parenchyma. As the weakest wall, it often fails in young trees lacking mature heartwood or under severe wounding, allowing vertical extension if plugging is incomplete.^[11] Wall 2, the radial barrier, consists of latewood cells at the end of each annual growth ring and marginal axial parenchyma, providing a physical boundary of thick-walled, lignified fibers that restricts decay spread perpendicular to the grain, inward toward the pith. This wall serves as a secondary defense, though it is less robust than later-formed barriers and can be breached if decay overwhelms the growth ring boundaries.^[11] Wall 3, the tangential barrier, functions as a maze-like structure between annual rings, primarily composed of ray parenchyma cells that form a lattice-like structure, enhanced by chemical modifications like suberization and phenolic accumulation. This pre-existing anatomy provides the strongest initial defense against circumferential (lateral) spread of decay around the trunk. Its discontinuous radial and longitudinal nature makes it effective at channeling decay into discrete compartments rather than allowing broad radial progression.^[11] Wall 4, the new radial barrier, emerges as a thick zone of parenchyma-like cells produced by the vascular cambium in subsequent growth seasons after wounding, often termed the barrier zone. This wall isolates entire wood compartments from pith to bark by depositing polyphenols, suberin, and denser tissue layers that separate pre-wound (infected) wood from newly formed healthy tissue. As the most effective long-term barrier, it requires significant energy investment but effectively confines decay over years, preventing reinvasion into vital sapwood. Recent research highlights the role of secondary metabolites, such as induced polyphenols, in reinforcing this barrier's chemical defenses.^[2] In terms of relative strength, Wall 4 is the strongest, followed by Wall 3, Wall 2, and then Wall 1, reflecting their developmental timing and anatomical durability—initial walls like 3 rely on existing robust parenchyma networks, while later walls like 4 build cumulative defenses but may thin over time. Failure modes highlight vulnerabilities: for instance, shake cracks, often associated with frost or mechanical stress, can breach Wall 1 by splitting along the grain, enabling rapid vertical decay progression in species like oaks. Such breaches underscore the model's emphasis on wound closure to bolster wall integrity.^[11]^[12]

Wound Response Dynamics

Upon injury, trees initiate an immediate wound response within hours to days, primarily through the release of phenolic compounds such as gallic acid and tannic acid, along with enzymes that oxidize cellular contents to form antimicrobial barriers.^[1] These chemicals impregnate cell walls and occupy cell interiors, sealing off vascular elements like vessels and tracheids to prevent microbial invasion and discoloration of surrounding wood.^[1] This rapid chemical defense strengthens pre-existing compartment boundaries, marking the onset of compartmentalization without repairing the damaged tissue.^[12] The progressive formation of compartmentalization walls follows a temporal sequence, beginning with Walls 1 and 2 as immediate responses that plug vertical and radial pathways through ballooning parenchyma cells and encrustations.^[1] Over weeks, Wall 3 develops via enhanced ray parenchyma activity, providing lateral resistance through cell differentiation.^[12] Wall 4, the strongest barrier, emerges over years through cambial proliferation and suberization, creating a suberin-lined zone that isolates new wood from the wound site.^[1] This sequence culminates in the four barrier walls, which collectively confine decay without allowing tissue regeneration.^[12] Several factors influence the efficiency of this wound response, including wound size, which correlates with greater decay extent in larger injuries due to increased exposure.^[12] Tree age affects column development, as older trees with established heartwood may limit vertical spread more effectively than younger ones.^[12] Species differences, such as those between diffuse-porous trees (e.g., maple) with terminal parenchyma enhancing radial barriers and ring-porous trees (e.g., oak) relying on earlywood vessels, further modulate response vigor and wall integrity.^[1] In successful compartmentalization, outer walls enable recolonization by allowing new vascular tissues to form over decayed compartments, supporting continued growth while the inner decayed wood persists without further spread.^[12] This process confines pathogens to the wood present at wounding, preventing systemic invasion as the tree reallocates resources to boundary reinforcement.^[1]

Applications and Implications

Tree Management Practices

Pruning practices informed by the compartmentalization of decay in trees (CODIT) model emphasize techniques that preserve the tree's natural barrier formation to limit decay spread. Guidelines recommend making cuts at the branch collar—a swollen area of specialized cells at the branch base—to minimize disruption to the barrier zone and promote rapid wound closure.^[13] Flush cuts, which remove the branch collar entirely, are discouraged as they enlarge wound exposure, damage protective tissues, and increase susceptibility to decay fungi by impairing wall formation.^[13] To execute safe pruning, a three-step method is advised: first, undercut the branch about one-third through and 12-18 inches from the trunk to prevent bark tearing; second, cut above the undercut to remove the branch weight; and third, make the final cut just outside the branch collar.^[14] Pruning during the dormant season (late fall to early spring) further supports CODIT by reducing infection risk when trees are less active and barriers develop more effectively.^[15] Wound dressings, such as paints or sealants applied to pruning cuts or injuries, have been shown to be ineffective and are not recommended, as they interfere with the CODIT process by trapping moisture, providing a nutrient source for pathogens, and preventing natural callus formation and barrier development.^[15] Research by Alex Shigo demonstrated that these materials crack over time, creating entry points for fungi and ultimately exacerbating decay rather than preventing it.^[15] Instead, management focuses on clean, proper cuts and allowing the tree to compartmentalize naturally without artificial interventions.^[14] Species-specific variations in CODIT efficiency influence tree selection and maintenance strategies in landscapes. Oaks, for instance, exhibit strong Wall 4 formation—longitudinal barriers that effectively confine decay to wood present at the time of wounding—making them resilient to vertical spread in urban settings.^[12] In contrast, maples often develop weaker longitudinal barriers, allowing greater potential for decay column extension, which informs cautious pruning and site placement to avoid stress that could compromise compartmentalization.^[12] These differences, documented through dissection studies of wounded trees, guide arborists in prioritizing species with robust defenses for high-risk environments.^[12] Integrating CODIT principles with integrated pest management (IPM) for decay fungi involves proactive monitoring of fruiting bodies, such as brackets or conks, to assess compartmentalization status without resorting to unnecessary chemical or invasive treatments that could disrupt barriers.^[14] This approach emphasizes cultural practices like maintaining tree vigor through proper watering and mulching to enhance natural defenses, while avoiding over-intervention that might create additional wounds and promote fungal ingress.^[14] Regular inspections allow for targeted actions only when decay threatens stability, preserving the tree's ability to isolate pathogens effectively.^[14]

Hazard Assessment and Research

Hazard assessment in trees relies on the CODIT model to evaluate the extent of decay and the integrity of compartmentalization barriers, enabling arborists to predict structural failure risks. Visual indicators such as conks, mushrooms, cavities, and nesting holes on trunks, branches, or roots signal active decay processes that may compromise barrier walls, particularly when combined with evidence of carpenter ant activity in affected wood. These external signs help identify breaches in Walls 1 through 4, guiding decisions on tree removal or intervention to mitigate hazards like branch or trunk failure.^[16] Advanced non-destructive tools like the Resistograph enhance CODIT-based assessments by drilling into wood to measure resistance, revealing the density and extent of decay without significant damage to the tree. This allows for precise evaluation of wall integrity, such as the strength of Wall 4 barrier zones, and quantifies decay volume to assess failure probability in high-risk urban settings. The device produces graphical outputs that correlate low resistance readings with decayed areas, supporting quantitative risk ratings in professional tree evaluations.^[17]^[18] Edward F. Gilman's research in the 1990s and early 2000s examined how leaf mass and wind loads affect CODIT effectiveness in urban trees, demonstrating that excessive canopy density increases branch sway and failure risk during storms. His studies on species like live oak showed that high leaf mass amplifies wind forces, potentially overwhelming compartmentalization barriers and leading to codominant stem failures if not addressed through targeted pruning. This work highlighted how urban stressors, such as confined root zones, reduce a tree's ability to maintain strong Walls 2 and 4 under dynamic loads, informing hazard protocols for street trees.^[19] Post-2000 research has explored genetic variations in CODIT efficacy, revealing inter- and intra-species differences, such as weaker reaction zones in Betula species due to fewer parenchyma cells, while hybrids like those in Populus show variable healing based on genetic stock.^[20]^[10]^[21] Studies also indicate that environmental stresses like drought can increase decay susceptibility by affecting tree vigor and hydraulic function, though specific impacts on barrier formation require further research.^[22] Despite its utility, the CODIT model has limitations in addressing abiotic stresses beyond wounding, such as lightning strikes, which can shatter tissues and bypass barriers without initiating typical decay patterns. It primarily focuses on macroscopic responses to biotic threats, overlooking molecular signaling and seasonal vulnerabilities like dormant-period inefficacy against fungal ingress. Researchers advocate for updated models incorporating molecular biology to elucidate cellular defenses, secondary metabolite production, and whole-tree hydraulic trade-offs, enabling a more comprehensive framework for future hazard predictions.^[23]^[2]^[24]

References

[1]
[PDF] Compartmentalization of decay in trees - Forest Service
The first part of the model represents the responses the tree makes at the time of the injury. In es- sence the tree strengthens walls that are already in place ...
[2]
Using the CODIT model to explain secondary metabolites of xylem ...
CODIT is a concept showing how trees are highly compartmented perennial organisms formed of discrete 3-D units that when under threat from any abiotic or biotic ...
[3]
[PDF] Tree Decay - AgEcon Search
theory of spontaneous generation, scientists believed that. Decay Caused Fungi. Robert Hartig, in tune with the germ theory that emerged after 1845, said that.Missing: microbial | Show results with:microbial
[4]
[PDF] Introduction To Urban Wood Decay Fungi 1
Causes of Wood Decay. In 1874 Robert Hartig, the father of forest pathology, proved that decay did not cause fungi! In fact, all decay of living trees of any ...Missing: 1901 germ theory
[5]
Text-book of the diseases of trees - Biodiversity Heritage Library
Oct 20, 2009 · Title. Text-book of the diseases of trees. Title Variants. Alternative: Textbook of the diseases of trees. By. Hartig, Robert, 1839-1901Missing: wood- decay germ theory
[6]
[PDF] Horticulture - RNZIH
Thus began many years of work which involved the dissecting of over 10,000 trees and the development of a new concept of how trees inhibit decay. Dr Shigo ...
[7]
[PDF] TREE DECAY - USDA Forest Service
Tree decay involves the tree's response to wounding, the digestion of cell walls, and the interaction of trees and microorganisms, starting with a wound.Missing: microbial | Show results with:microbial
[8]
[PDF] Compartmentalization of decay in trees
The CODIT system is based on two major points. First, a tree is a highly compartmented plant. Second, after a tree is wounded, the resulting defects are.<|control11|><|separator|>
[9]
[PDF] Compartmentalization - Maple Research
The model is called CODIT, an acronym for compartmentalization of decay in trees (117). Like compartmentalization, the model has two parts. Part 1 is ...
[10]
[PDF] Compartmentalization Of Decay In Trees
The CODIT model is a natural defense system, which prevents decay organisms from spreading throughout the wood, and. Page 3. BTRL. TR-18. 3 ensures survival of ...
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The Parenchyma of Secondary Xylem and Its Critical Role in Tree ...
Nov 9, 2016 · The CODIT model is made up of four 'so-called' walls in two-parts (Figure 2), which are conceptual and explain the anatomical divisions or ...
[12]
None
### Summary of Compartmentalization of Decay in Trees (CODIT)
[13]
A Few Tree Pruning Basics - UNH Extension
Feb 24, 2020 · Different from animals, plants don't heal wounds, but wall off damaged areas by creating a barrier around the injury site. Dr. Alex Shigo, (1930 ...
[14]
Wood Decay Fungi in Landscape Trees - UC IPM
Several fungal species can infect and rot trees. · The fruiting bodies of wood decay fungi, such as mushrooms, brackets, or conks, can help with identification.
[15]
[PDF] The Myth of Wound Dressings: - Washington State University
Although Shigo debunked the myth of wound dressing decades ago, it still persists, particularly among those with something to sell.
[16]
Understanding the Spread of Decay in Trees - Penn State Extension
Nov 10, 2024 · The CODIT model explains how trees react to wounds by developing or forming four walls or barriers designed to slow the spread of decay internally.
[17]
Resistance recording drills for decay assessment | Bartlett
Resistance recording drills or resistographs are tools used to evaluate decay and other defects in tree stems and branches as part of advanced tree risk ...
[18]
Decay in Trees and the Resistograph® - RINNTECH
The Resistograph is a resistance drill used to detect decay in wood, helping to determine the likelihood of tree failure by collecting and analyzing data.
[19]
Ed Gilman Pruning Research Update: Reduction Pruning to Prevent ...
Aug 29, 2014 · Gilman does Extension outreach to municipal arborists and urban foresters to teach pruning practices based on his research findings. Because he ...Missing: F. CODIT leaf mass 1990s
[20]
Variation in compartmentalisation ability - Arboriculture
Jan 20, 2016 · There exists both intra- and inter-species variation in relation to the efficacy of the compartmentalisation process – no one individual is ...
[21]
The Parenchyma of Secondary Xylem and Its Critical Role in Tree ...
The CODIT model is made up of four 'so-called' walls in two-parts (Figure 2), which are conceptual and explain the anatomical divisions or compartments that ...
[22]
(PDF) Using the CODIT model to explain secondary metabolites of ...
We also raise the limitations of the CODIT model and suggest its modification, encompassing other defence theory concepts. We envisage the development of a new ...Missing: lightning | Show results with:lightning
[23]
Effects of lightning on trees: A predictive model based on in situ ...
Sep 12, 2017 · This study provides the first quantitative mechanism describing how differences among trees can influence lightning–tree interactions.