Auxin degradation

ABA inhibits the enhancement of elongation by auxin, and there is evidence that ABA can inhibit auxin biosynthesis. ABA appears to reduce lAA levels during the regeneration of a physiological tip in decapitated coleoptiles (Anker 1975), and there is evidence for ABA-enhanced auxin degradation in the presence of supraoptimal concentrations of lAA (Milborrow 1966). 

XiE, Q., et al., SINAT5 promotes ubiquitin-related degradation of NACl to attenuate auxin signals. Nature, 2002, 419(6903), 167-70. 

Chloro-3-methyl-4-nitro-lH-pyrazole (Release) has no auxin-, gib-berellin-, or cytokinin-like activity, yet it is an ejffective abscission agent. At the present, there is no evidence to indicate that Release retards auxin, gibberellin, or cytokinin activity. It does stimulate and enhance the tissue production of ethylene (105). Release is fairly stable, and there is no indication that it is degraded by the tissue to ethylene per se (106). 

A major factor leading to abscission is the weakening of the middle lamella, cell walls, or cells in a separation zone across the petiole, pedicel, or stem. Although any of the known plant hormones can alter the progress of abscission, ethylene remains unique as the principal stimulus of the increased activity of wall-degrading enzymes in abscission, whereas auxin can be given a central role in the retardation of abscission. With the present level of understanding, it would seem that abscission control involves interactions between auxin and ethylene. 

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