Model depicting the role of SIZ1 in (i) SNC1-dependent auto-immunity and (ii) thermosensory growth via COP1 and PIF4.
Figures are generally photos, graphs and static images that would be represented in traditional pdf publications.
(A) Wild type situation; SIZ1 inhibits at the transcription and/or protein level SNC1-dependent auto-immunity (route a.). This involves PAD4, EDS1, SA accumulation, and transcriptional feedback regulation. SNC1 auto-immunity is suppressed at 28°C by PIF4 function, at least for the mutant snc1-1 (route b.) . SIZ1 sumoylation of COP1 stimulates the intrinsic ubiquitin (Ub) E3 ligase activity of COP1 resulting in degradation of COP1 substrates, including HY5 and SIZ1 [34,35] (route c.). In this way, SIZ1 amplifies and tunes COP1 activity at high temperature and/or dark conditions (based on Fig 4). (B) In the siz1-2 mutant, auto-immunity is not inhibited at low and only partially at high temperature. This results in enhanced resistance to bacteria in siz1-2 at low and high temperature, while requiring EDS1 and SNC1 function (Fig 3). COP1 activity is required to convey thermosensing resulting in less hypocotyl elongation growth in cop1-4 mutant (Fig 4C). This (residual) COP1 activity is reduced when SIZ1 is mutated (based on Fig 4C; [34,35]). As inhibition of snc1-1 auto-immunity at high temperature requires PIF4 function, it appears that route b. is compromised or absent in the siz1-2 mutant. The blue/red/black arrows depict signalling routes at 22°C, 28°C, or that are independent of these temperatures, respectively. The thickness of the arrows marks the amount of protein activity.