Heat stress upregulates G-T mismatch binding activities in zebrafish (Danio rerio) embryos preexposed and nonexposed to a sublethal level of cadmium (Cd).

G-T mispair frequently appears in eukaryotic DNA due to the spontaneous deamination of 5-methylcytosine paired with guanine and is therefore an important target for DNA mismatch repair (MMR). Our earlier studies showed the downregulation of G-T binding activities in cadmium (Cd)-exposed (Danio rerio) embryos. Since elevation of water temperature was reported to increase Cd toxicity in zebrafish, this study explored whether heat stress affected zebrafish mismatch binding capacity in the absence or presence of Cd. Heat stress (37 °C for 30 min) induced heat shock protein 70 mRNA expression in embryos at 10 and 24 h post fertilization (hpf). Heat stress weakly upregulated normal G-T sensing machinery and inhibited G-T recognition activity in embryos preexposed to 3 μM Cd for 9 h. Either heat shock or a 23-h Cd treatment alone caused a 1.7-fold stimulation of G-T binding capacity in 24 hpf embryos and heat stress of Cd-preexposed embryos further enhanced G-T binding activity to 2.5 fold of control. Normal and Cd-downregulated loop binding activities in 10 and 24 hpf embryos were almost unreactive to heat shock. Heat stress-upregulated G-T sensing in nonexposed, but not in Cd-preexposed, 24 hpf embryos correlated with stronger gene activities encoding MMR-linked mismatch detecting factors MutS homolog 2 and 6 plus a higher DNA binding activity of the transcription factor Sp1 that regulates msh2/msh6 expression. Our results suggested the importance of heat shock response in facilitating the correction of G-T mismatch in developing zebrafish even under Cd exposure.