During the last decade, several studies have focused on the effect that temperature has on Post Transcriptional Gene Silencing (PTGS).

With an interesting approach, the paper by Zhong et al. (2013) has revealed that a 13-day treatment at 30 °C is capable of releasing the PTGS in A. thaliana with a transgenerational effect.

https://www.pnas.org/content/p...

Moreover, this research group - headed by Zu-Hua He -, has recenlty deciphered the molecular network underlaying this heat-induced response. 

https://www.nature.com/articles/s41422-019-0145-8

They proposed a model in which the transgenerational thermomemory is mediated by a regulatory loop between HSFA2 (a heat-shock factor) and REF6 (a demethylase) in Arabidopsis. Long-term heat exposure may activate unknown plant heat sensor(s) that upregulate(s) HSFA2, which in fact targets and activates REF6 demethylase and the chromatin remodeler complex BRM. REF6/BRM are able to trigger H3K27me3 demethylation to activate HSFA2. Therefore, REF6 and HSFA2 form a heritable transcriptional feedback loop in heat responses and memory. Then, this regulatory loop activates the E3 ligase SGIP1, to trigger the transgenerational degradation of a key enzime in dsRNA production,SGS3, leading to the suppression of tasiRNA biosynthesis. Both the REF6-HSFA2 loop and the reduced tasiRNA levels converge to activate HTT5, which coordinates early flowering with decreased disease resistance in heat-stressed plants and their progeny.

However, some questions remain to be answered.

For example:

Would this system be useful to avoid PTGS in any transgenic line?

Would the supression of PTGS be a limitation for RNAi techonolgy, since it implies the action of SGS3 for response amplification?

Is it possible that, in a hypothetical patoghen-free environment, high temperatures trigger a greater seed production and represent a adaptative advantage?