Figure 7.

MYC2/MYC4 genetically interact with PIFs.

(A) Mutant plants (phyB, pifq, myc2myc4, phyBmyc2myc4, pifqmyc2myc4) were grown in WL until 4 weeks of age. Scale bar, 5 cm.

(B) Inflorescence stem length in various mutants. Tukey’s HSD test (∗∗P < 0.01) was used for statistical analysis, n > 10, mean ± SD.

(C) Transmission electron micrographs of stem cross sections showing interfascicular fiber cells. Scale bar, 5 μm.

(D) Statistics of SCW thickness in interfascicular fiber cells in (C). Data were collected from three biological replicates, and more than 10 cells were measured per biological replicate. Tukey’s HSD test (∗∗P < 0.01) was used for statistical analysis, mean ± SD.

(E and F) Expression of the key SCW regulatory (NST1) and biosynthesis-related (4CL1 and IRX8) genes in mutant plants. Analysis was performed on three biological replicates. Student’s t-test (∗∗P < 0.01, ∗P < 0.05) was used for statistical analysis, mean ± SD.

(G) WL enhances SCW thickening in fiber cells of the inflorescence stem. Under WL (high R:FR), PHYB is activated to its Pfr form, which enters the nucleus to inhibit PIF activity, and MYC2 is available to bind to the NST1 promoter to activate the NST1-directed SCW thickening process. In the shade (low R:FR), PHYB reverts to its inactive Pr form. PHYB cannot enter the nucleus, and PIF proteins interact with MYC2, displacing its binding to the NST1 promoter. Thus, the NST1-directed SCW thickening process is suppressed.