Figure 8.

Models for modulation of ethylene growth responses by GA in Arabidopsis, rice, and millet. In Arabidopsis, this model proposes that in the absence of ethylene, EIN2 levels are low so there are no ethylene responses and growth is fast. Growth rate is modulated by feedback control of GA levels where a higher growth rate leads to lower levels. Ethylene leads to an accumulation of EIN2. One output of EIN2 reduces growth via an EIN3/EIL1-independent mechanism. On a slower time course, this reduced growth leads to an increase in GA levels resulting in an increase in growth. This pathway is proposed to underlie the transient first phase of growth inhibition response. On a slower time course, EIN2 also inhibits degradation of EIN3/EIL1 mediated by the EBF1 and EBF2 F-box proteins. Accumulation of EIN3 and EIL1causes a lower growth rate leading to the second phase of prolonged growth inhibition response. Our results indicate that this is occurring via a GA-dependent pathway where EIN3 and EIL1 inhibit GA accumulation. There also is likely to be a GA-independent pathway. Thus, when EIN3 and EIL1 are not present, ethylene initially causes growth inhibition, but this inhibition is reversed by the delayed feedback involving GA. The model predicts that in rice, OsEIN2 activation by ethylene has no growth inhibition effect. On a slower time scale, activation of OsEIN2 leads to enhanced degradation of OsEIL1 and OsEIL2 mediated by the OsFBL7 and OsFBL30 F-box proteins. This leads to lower levels of OsEIL1 and OsEIL2, resulting in higher levels of GA and enhanced growth. In millet, the model proposes that PmEILs are either absent or at very low levels. Thus, PmEIN2 activity initially leads to growth inhibition, but feedback resulting in higher GA levels reverses this inhibition leading to a transient growth response.