Aluminum toxicity in plant cells: Mechanisms of cell death and inhibition of cell elongation

Abstract

ABSTRACT Aluminum (Al) ions are a major constraint for crop productivity in acidic soils. The root apex is the most sensitive plant part to Al, which inhibits root elongation and causes cell death. To elucidate the mechanisms of these toxic events, Al responses have been investigated in cultured cell lines of tobacco (Nicotiana tabacum), SL and BY-2. These cells at the logarithmic growth phase serve as a model system of meristematic cells at the root apex. Our research group has revealed three types of cell death mechanisms triggered by Al: (i) Enhancement of iron (Fe)-mediated lipid peroxidation leading to a loss of plasma membrane integrity (plasma membrane pathway); (ii) dysfunction of mitochondria accompanied by ROS production (mitochondria pathway); and (iii) upregulation of NtVPE1 encoding a vacuolar processing enzyme (VPE), which leads to vacuolar collapse and the loss of plasma membrane integrity (vacuole pathway). Mechanisms (ii) and (iii) have been confirmed in root systems of pea and tobacco seedlings, respectively. The inhibition of elongation (expansion) in SL cells was detected as a decrease in water content, together with decreased osmolality and soluble sugar content, which was partly due to the inhibition of sucrose uptake by Al. The inhibition of root elongation by Al due to the inhibition of the sucrose transporter (SUT) NtSUT1 localized at the plasma membrane was confirmed in tobacco seedlings, in which overexpression of NtSUT1 mitigated both the inhibition of elongation and cell death at the root apex under Al stress.