Bcl-2 suppresses activation of VPEs by inhibiting cytosolic Ca2+ level with elevated K+ efflux in NaCl-induced PCD in rice

• Bcl-2 suppresses NaCl-induced transient elevations in the cytosolic Ca2+ levels.
• Bcl-2 inhibits NaCl-induced K+ efflux across the plasma membrane.
• Bcl-2 acts like a NSCC blocker La3+ in suppressing NaCl-induced PCD.
• Bcl-2 and La3+ suppress NaCl-induced activation of vacuolar-processing enzymes.

Bcl-2 is one of the most important antiapoptotic members in mammals and prevents many forms of apoptosis in a variety of cell types. Our previous study revealed that overexpression of Bcl-2 significantly suppressed H2O2/NaCl-induced programmed cell death via inhibiting the transcriptional activation of OsVPE2 and OsVPE3 in transgenic rice. However, Ca2+ and K+ homeostasis of this process remains largely unknown. In the present study, we investigate whether nonselective cation channels (NSCC) blockers affect Bcl-2 function in rice under salt stress and how Bcl-2 affects ion homeostasis in salt stress-induced PCD. The results showed that overexpression of Bcl-2 significantly decreased transient elevations in the cytosolic Ca2+ levels, inhibited NaCl-induced K+ efflux but not H+ efflux across the plasma membrane, and further suppressed the expression levels of OsVPE2 and OsVPE3, leading to the inhibition of salt-induced PCD and increase of tolerance to salt stress in transgenic rice. During the NaCl-induced PCD, the effects of a NSCC blocker La3+ on ion homeostasis and VPEs expression in wild-type were similar to the effects of Bcl-2 overexpression in transgenic line. However, a synergistic effect of Bcl-2 and La3+ was not obviously detectable. Our results suggested that Bcl-2 played an important role in suppression of NaCl-induced PCD by disruption of ion homeostasis, providing an insight into the mechanistic study of plant VPEs, cytosolic Ca2+ level and K+ efflux.