Mouse-ear (ME) is a potentially severe anomalous growth disorder affecting young pecan [Carya illinoinensis (Wangenh.) K. Koch] trees in portions of the Gulf Coast Coastal Plain of the southeastern United States. A survey of its incidence and severity found it to be commonly exhibited by replants on second-generation orchard sites, or where mature pecan trees previously grew. While most frequently observed as a replant problem, it also occasionally occurs at sites where pecan has not previously grown. The disorder is not graft transmissible and is only temporarily mitigated by pruning. Degree of severity within the tree canopy typically increases with canopy height. Several morphological and physiological symptoms for mouse-ear are described. Important symptoms include dwarfing of tree organs, poorly developed root system, rosetting, delayed bud-break, loss of apical dominance, reduced photoassimilation, nutrient element imbalance in foliage, and increased water stress. The overall symptomatology is consistent with a physiological deficiency of a key micronutrient at budbreak, that is influenced by biotic (e.g., nematodes) and abiotic (e.g., water and fertility management strategies) factors. A comparison of orchard soil characteristics between ME and adjacent normal orchards indicated that severely affected orchards typically possessed high amounts of soil Zn, Ca, Mg, and P, but low Cu and Ni; and were acidic and sandy in texture. The Zn: Cu ratio of soils appears to be a major factor contributing to symptoms, especially since ME severity increases as the Zn: Cu ratio increases. However, Ni may also be a factor as the Zn: Ni ratio is also larger in soils of ME sites. It is postulated that the “severe” form of mouse-ear is primarily due to the physiological deficiency of copper at budbreak, but may also be influenced by Ni and nematodes.
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