From wikipedia:
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There are several signaling molecules that help the plant determine where the light source is coming from, and these activate several genes, which change the hormone gradients allowing the plant to grow towards the light. The very tip of the plant is known as the coleoptile, which is necessary in light sensing.[2] The middle portion of the coleoptile is the area where the shoot curvature occurs. The Cholodny–Went hypothesis, developed in the early 20th century, predicts that in the presence of asymmetric light, auxin will move towards the shaded side and promote elongation of the cells on that side to cause the plant to curve towards the light source.[5] Auxins activate proton pumps, decreasing the pH in the cells on the dark side of the plant. This acidification of the cell wall region activates enzymes known as expansins which disrupt hydrogen bonds in the cell wall structure, making the cell walls less rigid. In addition, increased proton pump activity leads to more solutes entering the plant cells on the dark side of the plant, which increases the osmotic gradient between the symplast and apoplast of these plant cells.[6] Water then enters the cells along its osmotic gradient, leading to an increase in turgor pressure. The decrease in cell wall strength and increased turgor pressure above a yield threshold[7] causes cells to swell, exerting the mechanical pressure that drives phototropic movement.
Proteins encoded by a second group of genes, PIN genes, have been found to play a major role in phototropism. They are auxin transporters, and it is thought that they are responsible for the polarization of auxin location. Specifically PIN3 has been identified as the primary auxin carrier.[8] It is possible that phototropins receive light and inhibit the activity of PINOID kinase (PID), which then promotes the activity of PIN3. This activation of PIN3 leads to asymmetric distribution of auxin, which then leads to asymmetric elongation of cells in the stem. pin3 mutants had shorter hypocotyls and roots than the wild-type, and the same phenotype was seen in plants grown with auxin efflux inhibitors.[9] Using anti-PIN3 immunogold labeling, movement of the PIN3 protein was observed. PIN3 is normally localized to the surface of hypocotyl and stem, but is also internalized in the presence of Brefeldin A (BFA), an exocytosis inhibitor. This mechanism allows PIN3 to be repositioned in response to an environmental stimulus. PIN3 and PIN7 proteins were thought to play a role in pulse-induced phototropism. The curvature responses in the "pin3" mutant were reduced significantly, but only slightly reduced in "pin7" mutants. There is some redundancy among "PIN1", "PIN3", and "PIN7", but it is thought that PIN3 plays a greater role in pulse-induced phototropism.[10]
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