2.6 BES1 is required for sustained activation of HS-associated
memory genes
To analyze whether BES1 mediates thermomemery through affecting the
expression of HS-associated memory genes, we examined the transcript
level of memory genes in thermomemory assay at the indicating time
point. The HS memory‐associated genes APX2 (Stief et al., 2014a),HSFA3 (Friedrich et al., 2021), HSA32 (Wu et al., 2013),HSP21 (Sedaghatmehr, Mueller-Roeber, & Balazadeh, 2016) were
analyzed (include both type I and type Ⅱ HS-associated memory gene) and
a non‐memory but HS‐inducible gene HSP101 (McLoughlin et al.,
2019) was set as contrast. These genes did not show dramatic differences
among Col-0, bes1-D and BES1-RNAi prior priming (Fig. 5A),
indicating that BES1 has a weak regulatory effect on these genes under
normal growth conditions. The expression of APX2 , HSFA3and HSP21 was induced several hundred-fold (Fig. 5B, D and E) andHSA32 for several dozen fold (Fig. 5C) early in the memory phase
and sustained relative high transcript level 3 d after priming in
wild-type and bes1-D . These genes were less induced inBES1-RNAi mutant early in the memory phase and later decreased
faster than Col-0 and bes1-D . With the deepening of memory phase,
the expression of these memory genes started to decrease between 12 and
24 h and declined dramatically 48 h after priming in BES1-RNAiwhen it was still relatively high in Col-0 and bes1-D . For the
non‐memory gene HSP101 , no significant difference was found among
Col-0, bes1-D and BES1-RNAi during the memory phase (Fig.
5F). These results indicate that BES1 is required to a great extent for
sustained activation of HS memory‐associated genes.