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At the molecular level, auxin and gibberellins act similarly

The molecular mechanisms underlying both auxin and gibberellin action have been worked out with the help of genetic screens (see Figure 36.2). Biologists started by identifying mutant plants whose growth and development are insensitive to the hormones—that is, plants that are not affected by added hormone. Such mutant plants fall into two general categories:

Excessively tall plants. These plants resemble wild-type plants given an excess of hormone and grow no taller when given extra hormone. They grow tall even when treated with inhibitors of hormone synthesis. Their hormone response is always “on,” even in the absence of the hormone. In such cases, it is presumed that the normal allele for the mutant gene codes for an inhibitor of the hormone signal transduction pathway. In wild-type plants, that pathway is “off,” but in the mutant plants, the pathway is “on” and the plant grows tall.
Dwarf plants. These plants resemble dwarf plants that are deficient in hormone synthesis (see Figure 36.3), but they do not respond to added hormone. In these mutant plants the hormone response is always “off,” regardless of the presence of the hormone.

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Remarkably, some mutations of both types turned out to affect the same protein, which turns out to be a repressor of a transcription factor that stimulates the expression of growth-promoting genes. The repressor protein has two important domains, which explains how mutations in the same protein can have seemingly opposite effects:

One region of the repressor protein binds to the transcription complex to inhibit transcription of growth-promoting genes. This is the region mutated in the excessively tall plants: the growth-promoting genes are always “on” because the repressor does not bind to the transcription complex.
Another region of the repressor protein causes it to be removed from the transcription complex. This is the region mutated in the dwarf plants: the growth-promoting genes are always “off” because the repressor is always bound to the complex.

These observations allowed biologists to figure out how auxin and gibberellins work in wild-type plants. The repressor proteins involved in responding to the two hormones are different, but both hormones act by removing the repressor from the *transcription complex (Focus: Key Figure 36.10). The hormones do this by binding to a receptor protein, which in turn binds to the repressor. Binding of the hormone–receptor complex stimulates polyubiquitination of the repressor, targeting it for breakdown in the proteasome (see Figure 16.20). The receptors contain or associate with a region called an F-box that facilitates protein–protein interactions necessary for polyubiquitination of a target protein. Whereas animal genomes have few F-box-containing proteins, plant genomes have hundreds, an indication that this type of gene regulation is common in plants.

*connect the concepts Key Concept 16.2 explains how transcription factors bind to DNA and affect the rate of transcription in the regulation of gene expression.

focus: key figure

Figure 36.10 Gibberellins and Auxin Have Similar Signal Transduction Pathways Although the specific proteins involved are different, both hormones act to stimulate gene transcription by inactivating a repressor protein.

Question

Q: Are the molecules (receptor, repressor, transcription factor, ubiquitin, proteasome) the same or different in auxin versus gibberellin signaling?

Only ubiquitin and proteasome are the same. The other molecules are specific to the particular hormone. For example, there is a specific receptor for auxin and a different receptor for gibberellin.

Media Clip 36.1 Gibberellin Binding to Its Receptor

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