We investigated temperature responsiveness of res2 in context to various growth and developmental phenotypes at different temperatures. We found that res2 shows severely suppressed thermsoensory growth responses, particularly hypocotyl and rosette growth. Very interestingly, flowering phenotype of res2 mutant was comparable to wild-type both at 22°C and 27°C, suggesting that RES2 is probably not involved in controlling flowering time. We characterised key defense outputs such as the levels of Reactive oxygen species (ROS) generation upon perception of Pathogen associated molecular pattern (PAMP) such flg22; and res2 was found to to have increased levels of ROS at 22°C and 27°C. In order to map the res2 mutation, we performed bulk-seggregant RNA-seq analysis. While this has identified a number of potential candidate genes, RES2 could not be mapped in the stipulated time, possibly be due to still high number of background mutations. Efforts are underway to reduce the background mutations through repeated backcrosses. Following up on the attenuation of thermosensory growth responses in res2 in order to understand the molecular basis of the link between growth and immunity, we found that res2 suppressed PIF4-mediated temperature responses. We found that PIF4 singling is essential for the suppression of defense by elevated temperature. Moreover, PIF4 acts as a negative regulator of immunity in Arabidopsis. Modulation of PIF4 function in mutants or transgenics resulted in an altered balance between growth and defense. Importantly, reducing PIF4 singling led to resilient resistance against diseases at elevated temperatures (Gangapa et al., 2017), depicting a likely mechanism in res2. Plant growth in nature is controlled by a multiple environmental factors. We discovered that two upstream regulators, DE-ETIOLATED 1 (DET1) and CONSTITUTIVE PHOTOMORPHOGENESIS 1 (COP1), are essential to maintain PIF4 function. DET1 and COP1 are required to stabilize PIF4 protein levels. This provides a molecular mechanism whereby PIF4 activity and function is coordinately controlled by DET/COP1 and HY5 in context to light and temperature signals (Gangappa and Kumar 2017). Collectively, the characterization of res2 mutant for thermosensory growth and defense phenotypes suggest that res2 mutant has defective thermosensory response, which is due to reduced PIF4-signaling. Analysis of PIF4 signaling for growth and defense responses show that PIF4 plays a key role in coordinating growth and defense responses in context to temperature. Further, we show that natural variation in PIF4 signaling could contribute to the balance between growth and defense responses in natural wild-type Arabidopsis strains. We also able to demonstrate that manipulation of PIF4 signaling could be one of the ways through which resilient resistance can be obtained. Furthermore, we also discovered the regulatory mechanism through which PIF4 function is controlled in response to different environmental signals. Future research focusing on the mapping of the res2 mutation and characterization of RES2 for molecular and biochemical functions would further reveal how exactly RES2 cross-talk with PIF4-signaling in coordinating growth and defense responses in context to different environmental signals.
