Strigolactone-Regulated Hypocotyl Elongation Is Dependent on Cryptochrome and Phytochrome Signaling Pathways in Arabidopsis

Abstract

Seedling development including hypocotyl elongation is a critical phase in the plant life cycle. Light regulation of hypocotyl elongation is primarily mediated through the blue light photoreceptor cryptochrome and red/far-red light photoreceptor phytochrome signaling pathways, comprising regulators including COP1, HY5, and phytochrome-interacting factors (PIFs). The novel phytohormones, strigolactones, also participate in regulating hypocotyl growth. However, how strigolactone coordinates with light and photoreceptors in the regulation of hypocotyl elongation is largely unclear. Here, we demonstrate that strigolactone inhibition of hypocotyl elongation is dependent on cryptochrome and phytochrome signaling pathways. The photoreceptor mutants cry1 cry2, phyA, and phyB are hyposensitive to strigolactone analog GR24 under the respective monochromatic light conditions, while cop1 and pif1 pif3 pif4 pif5 (pifq) quadruple mutants are hypersensitive to GR24 in darkness. Genetic studies indicate that the enhanced responsiveness of cop1 to GR24 is dependent on HY5 and MAX2, while that of pifq is independent of HY5. Further studies demonstrate that GR24 constitutively up-regulates HY5 expression in the dark and light, whereas GR24-promoted HY5 protein accumulation is light- and cryptochrome and phytochrome photoreceptor-dependent. These results suggest that the light dependency of strigolactone regulation of hypocotyl elongation is likely mediated through MAX2-dependent promotion of HY5 expression, light-dependent accumulation of HY5, and PIF-regulated components.

The activities of the E3 ubiquitin ligase COP1/SPA, a key repressor in light signaling

“…Moreover, strigolactones inhibit hypocotyl elongation in a HY5-dependent fashion, implementing HY5 in the strigolactone response. Concomitantly, HY5 protein levels increase upon strigolactone treatment in light-grown seedlings [67,68]. This correlates with the observed reduced nuclear accumulation of GUS-COP1 in transgenic 35S:GUS-COP1 plants [67], though part of the strigolactone response on HY5 might also be caused by the strigolactone-induced increase in HY5 expression [67,68].…”

DET1 and HY5 Control PIF4-Mediated Thermosensory Elongation Growth through Distinct Mechanisms

“…These findings are consistent with the earlier studies suggesting that HY5 alone is not sufficient to explain the regulation of photomorphogenesis by DET1 and COP1(Ang and Deng, 1994, Chory, 1992, Fernando and Schroeder, 2015). Similarly, the hy5 pifq quintuple mutant (Jia et al., 2014) strongly phenocopied det1 hy5 and cop1 hy5 (Figures 2F and 2G), suggesting that DET1 and COP1 primarily act to maintain PIF function. Together, these results further confirm our hypothesis that DET1/COP1 and HY5 regulate temperature-induced elongation growth through independent mechanisms.…”

“…The hy5 mutants, hy5-215 (Datta et al., 2007) and hy5 (Jia et al., 2014) are in (Col-0), whereas hy5 ks-50 (Holm et al., 2002) and hy5-1 (Datta et al., 2007) are in Wassilewskija (Ws) and Landsberg erecta (Ler-0) ecotypes, respectively. The det1-1 , cop1-4 , cop1-6 , hy5 cop1-4 , hy5 det1 , and pifq hy5 mutants have been described previously (Fernando and Schroeder, 2015, Holm et al., 2002, Jia et al., 2014, Schroeder et al., 2002). det1-1 and cop1-4 were crossed to 35S:PIF4-HA (Nozue et al., 2007) to generate det1-1 35S:PIF4-HA and cop1-4 35S:PIF4-HA lines.…”

Karrikins: Regulators Involved in Phytohormone Signaling Networks during Seed Germination and Seedling Development

“…max2 mutants showed deep seed dormancy, epinastic leaves and long hypocotyls under white light, red light, far-red light, and blue light conditions (Nelson et al, 2011; Waters et al, 2012; Stanga et al, 2013; Jia et al, 2014). This suggests that MAX2 is a positive regulator of photomorphogenesis (Shen et al, 2007).…”