functional characterization of several genes including TFs and miRNAs that are
altered in response to stress suggest their involvement in the maintenance of stress
tolerance (Nelson et al. 2007; Sunkar et al. 2007; Petroni et al. 2012; Yan et al. 2013;
Baxter et al. 2014; Kumar et al. 2014; Lee et al. 2014; Golldack et al. 2014; Weng
et al. 2016; Zanetti et al. 2017; Zhou and Tang 2019; Liebsch and Palatnik 2020;
Millar 2020). Moreover, detailed analysis of several miRNA biogenesis mutants like
hyponastic leaves 1 (hyl1), cap-binding protein 80/aba hypersensitive 1 (cbp80/
abh1), and sickle (sic) under different abiotic stress conditions clearly suggests the
critical role of miRNAs in plant stress regulation (Lu and Fedoroff 2000; Kim et al.
2008; Zhang et al. 2008; Zhan et al. 2012). These alterations in TFs and miRNAs
levels in response to plant stress responses have revealed the existence of complex
regulatory networks that control the onset of different gene networks. Elucidation of
such networks is pivotal for understanding the molecular mechanisms of plants
stress response. Exploring the interplay between TFs and miRNAs will help in
understanding the organization of several stress responsive networks in plants,
some of which form feedback loop circuits. This chapter will provide deeper insights
into TF:miRNA:target mediated gene regulation and their crosstalk during plant
abiotic stress responses.
8.2
TFs-miRNAs: Regulating Plant Heat Stress Response
Global mean temperatures have seen an upsurge in the past few decades. Heat stress
(HS) is a major limiting factor in plant growth, development, and productivity.
Previously, heat stress transcription factors (HSFs) were considered as the key
players of plant heat stress response (HSR) regulating the expression of heatresponsive genes like heat shock proteins (HSPs) (Wang et al. 2004). However,
many non-coding RNAs including miRNAs have now been found to mediate plant
HSR also (Fig. 8.1 and Table 8.1). In Arabidopsis, miR398 has four target genes,
viz. copper/zinc superoxide dismutases 1 and 2 (CSD1 and CSD2), mitochondrial
cytochrome c oxidase (Cox5b-1), and CCS1 [copper chaperone for superoxide
dismutase (SOD)] (Sunkar and Zhu 2004). CSD proteins are important scavengers
of reactive oxygen species (ROS) and CSD/CCS negatively regulates the accumulation of different ROS species (Mittler et al. 2004; Sunkar et al. 2006). It has been
shown that under HS conditions, there is a rapid rise in the miR398 levels via direct
HSF-mediated (HSFA1b and HSFA7b) transcriptional regulation of MIR398
precursors (Guan et al. 2013). Downregulation of its targets CSD1, CSD2, and
CCS modifies the redox status of cells that is sensed by HSFs which in turn regulate
not only miR398 expression but also other HSR genes. The loss of function csd1,
csd2, and ccs Arabidopsis mutants are more heat tolerant and maintain higher HSF
and HSP levels while the miR398-resistant forms of target genes that avoid cleavage
by miRNAs are more sensitive to HS (Guan et al. 2013; Lu et al. 2013). This
miR398:CSDs/CCS module is also functional in the HS responses in Brassica
rapa and Populus tomentosa (Kotak et al. 2007; Yu et al. 2011), indicating that
the HSF:miR398:CSD/CCS pathway is widely conserved in the HS response in
8 Orchestration of MicroRNAs and Transcription Factors in the Regulation of Plant. . .
253
altered in response to stress suggest their involvement in the maintenance of stress
tolerance (Nelson et al. 2007; Sunkar et al. 2007; Petroni et al. 2012; Yan et al. 2013;
Baxter et al. 2014; Kumar et al. 2014; Lee et al. 2014; Golldack et al. 2014; Weng
et al. 2016; Zanetti et al. 2017; Zhou and Tang 2019; Liebsch and Palatnik 2020;
Millar 2020). Moreover, detailed analysis of several miRNA biogenesis mutants like
hyponastic leaves 1 (hyl1), cap-binding protein 80/aba hypersensitive 1 (cbp80/
abh1), and sickle (sic) under different abiotic stress conditions clearly suggests the
critical role of miRNAs in plant stress regulation (Lu and Fedoroff 2000; Kim et al.
2008; Zhang et al. 2008; Zhan et al. 2012). These alterations in TFs and miRNAs
levels in response to plant stress responses have revealed the existence of complex
regulatory networks that control the onset of different gene networks. Elucidation of
such networks is pivotal for understanding the molecular mechanisms of plants
stress response. Exploring the interplay between TFs and miRNAs will help in
understanding the organization of several stress responsive networks in plants,
some of which form feedback loop circuits. This chapter will provide deeper insights
into TF:miRNA:target mediated gene regulation and their crosstalk during plant
abiotic stress responses.
8.2
TFs-miRNAs: Regulating Plant Heat Stress Response
Global mean temperatures have seen an upsurge in the past few decades. Heat stress
(HS) is a major limiting factor in plant growth, development, and productivity.
Previously, heat stress transcription factors (HSFs) were considered as the key
players of plant heat stress response (HSR) regulating the expression of heatresponsive genes like heat shock proteins (HSPs) (Wang et al. 2004). However,
many non-coding RNAs including miRNAs have now been found to mediate plant
HSR also (Fig. 8.1 and Table 8.1). In Arabidopsis, miR398 has four target genes,
viz. copper/zinc superoxide dismutases 1 and 2 (CSD1 and CSD2), mitochondrial
cytochrome c oxidase (Cox5b-1), and CCS1 [copper chaperone for superoxide
dismutase (SOD)] (Sunkar and Zhu 2004). CSD proteins are important scavengers
of reactive oxygen species (ROS) and CSD/CCS negatively regulates the accumulation of different ROS species (Mittler et al. 2004; Sunkar et al. 2006). It has been
shown that under HS conditions, there is a rapid rise in the miR398 levels via direct
HSF-mediated (HSFA1b and HSFA7b) transcriptional regulation of MIR398
precursors (Guan et al. 2013). Downregulation of its targets CSD1, CSD2, and
CCS modifies the redox status of cells that is sensed by HSFs which in turn regulate
not only miR398 expression but also other HSR genes. The loss of function csd1,
csd2, and ccs Arabidopsis mutants are more heat tolerant and maintain higher HSF
and HSP levels while the miR398-resistant forms of target genes that avoid cleavage
by miRNAs are more sensitive to HS (Guan et al. 2013; Lu et al. 2013). This
miR398:CSDs/CCS module is also functional in the HS responses in Brassica
rapa and Populus tomentosa (Kotak et al. 2007; Yu et al. 2011), indicating that
the HSF:miR398:CSD/CCS pathway is widely conserved in the HS response in
8 Orchestration of MicroRNAs and Transcription Factors in the Regulation of Plant. . .
253