Research Projects

Warm ambient temperatures significantly accelerate plant growth and development by hastening vegetative and reproductive transitions, shortening the life cycle. However, these conditions adversely affect pollen development and plant defense responses, leading to substantial yield losses (Battisti and Naylor, 2009; Zhao et al., 2017). The genetic and molecular mechanisms underlying temperature perception and signaling integration have been elucidated in Arabidopsis (Casal and Balasubramanian, 2019). PHYTOCHROME INTERACTING FACTOR 4 (PIF4), a bHLH transcription factor, is pivotal in mediating responses to warm ambient temperatures. PIF4 directly activates several downstream genes essential for auxin biosynthesis, cell elongation, and flowering (Koini et al., 2009; Franklin et al., 2011; Kumar et al., 2012; Gangappa and Kumar, 2017). Several upstream regulators of PIF4 have been identified, which modulate its function by controlling PIF4 protein stability or regulating its transcription (Jung et al., 2016; Gangappa and Kumar, 2017; Park et al., 2017; Malakar et al., 2025; Das et al., 2025), indicating its central regulatory role in warm temperature signaling. The Polycomb Repressive Complex (PRC) is highly conserved across plant species and regulates postembryonic phase transitions, floral identity gene expression, and flower development through H3K27me3 epigenetic marks. The PRC comprises PRC1 and PRC2. PRC2, consisting of CURLY LEAF (CLF) and SWINGER (SWN) as methyltransferases, deposits H3K27me3 marks on chromatin. PRC1, with TERMINAL FLOWER 2 (TFL2), as a key component, recognizes and stabilizes these marks, leading to stable gene expression repression. While the role of PRC has been well documented in cold-temperature-induced regulation of flowering in a vernalization pathway, its role in warm-temperature signaling-mediated growth remains unknown. To investigate the potential role of the PRC, we screened the mutants of individual PRC components for warm temperature-induced hypocotyl growth. Notably, the tfl2 mutant exhibited a near temperature-insensitive hypocotyl growth phenotype (~110% increase) compared to the wild-type (Col-0), which showed a ~240% increase in hypocotyl growth. In contrast, clf, swn, ring1a, and ring1b mutants did not show any altered response in warm temperature-induced hypocotyl length under warm temperatures, likely suggesting these components have no role or minimal role, if any. Interestingly, the tfl2 mutant’s strong temperature-insensitive hypocotyl growth response was similar to that of the pif4 mutant, suggesting that TFL2 likely functions in the same pathway as PIF4, potentially promoting PIF4 activity or by activating the expression of PIF4-targeted downstream genes through an unknown mechanism. Hence, we propose elucidating the molecular mechanism by which TFL2 regulates warm temperature responses in Arabidopsis using a combination of genetic, genomic, and biochemical approaches.