The Ca ( 2+) /calmodulin (CaM) signaling pathway mediates the heat stress (HS) response and acquisition of thermotolerance in plants. We showed that the rice CaM1-1 isoform can interpret a Ca ( 2+) signature difference in amplitude, frequency, and temporal-spatial properties in regulating transcription of nucleoplasmic small heat-shock protein gene (sHSPC/N) during HS. Ca ( 2+) and A23187 treatments under HS generated an intense and sustained increase in [Ca ( 2+) ]cyt and accelerated the expression of CaM1-1 and sHSPC/N genes, which suggests that HS-induced apoplastic Ca ( 2+) influx was responsible for the [Ca ( 2+) ]cyt transient and downstream HS signaling. Here, we discuss an emerging paradigm in the oscillation regulation of CaM1-1 expression during HS and highlight the areas that need further investigation.
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| http://dx.doi.org/10.4161/psb.21124 | DOI Listing |
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