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  • Author or Editor: Lisa M. Blanchard x
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Sweet corn roots colonized with the T-22 strain of the common rhizosphere fungus grow substantially faster than roots of plants not so colonized. We tested whether this growth enhancement was a consequence of the fungus affecting auxin regulation of cell elongation. In corn roots, auxin acts an inhibitor of growth, maintaining the rate below its short-term maximum potential. The first hypothesis was that the fungus secretes an auxin inhibitor, and thereby reduces the auxin limitation of growth. Apical segments (5 cm) were incubated in media conducive to elongation, supplemented with 0.1 μm indole acetic acid (IAA), a T-22 culture filtrate (5%), or both. IAA inhibited growth by 69%, and the culture filtrate inhibited by 16% with no interaction. The action of T-22, therefore, is not through a secreted antiauxin. The second hypothesis was that the fungus metabolizes or otherwise reduces the effectiveness of auxin, which was tested by measuring growth of colonized and uncolonized seedlings after a half-hour incubation of the root tips in 0.1 μm IAA. Auxin inhibited growth by 42%, whereas colonization increased growth by 27%. Again, there was no interaction, a result inconsistent with the antiauxin model. The third experiment further tested the antiauxin hypothesis by maximizing acid growth (normally regulated by auxin) by incubating the root tips in 1 μm fusicoccin (FC). Colonization increased growth by 10% without FC but by 42% with it. FC alone increased growth by 11%. The significant positive interaction is not consistent with a change in the auxin sensitivity but is consistent with an increase in the maximum sustainable growth rate.

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Sweet corn (Zea mays L.) varieties carrying the sh2 gene are in high demand, but such varieties have poor stress tolerance, especially during plant establishment. Trichoderma harzianum Rifai strain 1295-22 is a biocontrol fungus developed to provide season-long colonization of crop roots. It has the potential to reduce root rot and increase root growth. In the absence of detectable disease, colonization by Trichoderma increased root and shoot growth by an average of 66%. The enhancement was not uniform among the plants. Low- and intermediate-vigor plants were larger in the presence of Trichoderma, but high-vigor plants were not further enhanced by the fungus. Seeds that were subjected to oxidative stress with 0.05% NaOCI had much-reduced vigor; subsequent treatment with Trichoderma fully restored vigor. This result indicates that the damage caused by hypochlorite is specifically repaired by Trichoderma. Treatment of imbibed but unemerged seeds with cold (5/10 °C night/day) for varying periods reduced subsequent growth. Plants with Trichoderma-colonized roots were 70% larger at all durations of cold treatment. The absence of interation indicates the growth reduction due to cold and the growth enhancement due to Trichoderma are by different mechanisms. Allelopathic reduction in root growth by rye was mimicked by applying benzoxazolinone to the soil. Trichoderma-colonized roots grew faster, but the characteristic shortening of the radicle still occurred. There was no interaction between Trichoderma and allelopathy, indicating that these two treatments affect growth by independent mechanisms. The different ways that growth was enhanced by Trichoderma lead us to propose that this fungus acts, in part, by reversing injurious oxidation of lipids and membrane proteins. Root growth is markedly enhanced by colonization with Trichoderma harzianum. This enhancement can restore some stress-induced growth reduction and may directly reverse oxidative injury.

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