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MSH2 and MSH6 in Mismatch Repair System Account for Soybean (Glycine max (L.) Merr.) Tolerance to Cadmium Toxicity by Determining DNA Damage Response.
Journal of Agricultural and Food Chemistry ( IF 6.1 ) Pub Date : 2020-02-05 , DOI: 10.1021/acs.jafc.9b06599 Qiang Zhao 1 , Hetong Wang 2 , Yanli Du 1 , Hilary J Rogers 3 , Zhixin Wu 1 , Sen Jia 1 , Xingdong Yao 1 , Futi Xie 1 , Wan Liu 4
Journal of Agricultural and Food Chemistry ( IF 6.1 ) Pub Date : 2020-02-05 , DOI: 10.1021/acs.jafc.9b06599 Qiang Zhao 1 , Hetong Wang 2 , Yanli Du 1 , Hilary J Rogers 3 , Zhixin Wu 1 , Sen Jia 1 , Xingdong Yao 1 , Futi Xie 1 , Wan Liu 4
Affiliation
Our aim was to investigate DNA mismatch repair (MMR) genes regulating cadmium tolerance in two soybean cultivars. Cultivars Liaodou 10 (LD10, Cd-sensitive) and Shennong 20 (SN20, Cd-tolerant) seedlings were grown hydroponically on Murashige and Skoog (MS) media containing 0-2.5 mg·L-1 Cd for 4 days. Cd stress induced less random amplified polymorphism DNA (RAPD) polymorphism in LD10 than in SN20 roots, causing G1/S arrest in LD10 and G2/M arrest in SN20 roots. Virus-induced gene silencing (VIGS) of MLH1 in LD10-TRV-MLH1 plantlets showed markedly diminished G1/S arrest but enhanced root length/area under Cd stress. However, an increase in G1/S arrest and reduction of G2/M arrest occurred in SN20-TRV-MSH2 and SN20-TRV-MSH6 plantlets with decreased root length/area under Cd stress. Taken together, we conclude that the low expression of MSH2 and MSH6, involved in the G2/M arrest, results in Cd-induced DNA damage recognition bypassing the MMR system to activate G1/S arrest with the assistance of MLH1. This then leads to repressed root growth in LD10, explaining the intervarietal difference in Cd tolerance in soybean.
中文翻译:
失配修复系统中的MSH2和MSH6通过确定DNA损伤反应来解释大豆(Clycine max(L.)Merr。)对镉毒性的耐受性。
我们的目的是研究调节两个大豆品种对镉的耐受性的DNA错配修复(MMR)基因。在含0-2.5 mg·L-1 Cd的Murashige和Skoog(MS)培养基上,水L生长的辽都10号品种(LD10,对Cd敏感)和神农20(SN20,对镉耐受)。镉胁迫在LD10中引起的随机扩增多态性DNA(RAPD)多态性少于SN20根,导致LD10中的G1 / S阻滞和SN20根中的G2 / M阻滞。LD10-TRV-MLH1幼苗中MLH1的病毒诱导基因沉默(VIGS)显示,镉胁迫下G1 / S阻滞明显减少,但根长/面积增加。然而,SN20-TRV-MSH2和SN20-TRV-MSH6幼苗的G1 / S停滞增加和G2 / M停滞的减少在Cd胁迫下根长/面积减小。综上所述,我们得出的结论是,MSH2和MSH6的低表达,参与G2 / M逮捕,导致Cd诱导的DNA损伤识别绕过MMR系统,借助MLH1激活G1 / S逮捕。然后,这导致LD10的根生长受到抑制,从而解释了大豆对Cd的耐受性的种间差异。
更新日期:2020-02-06
中文翻译:
失配修复系统中的MSH2和MSH6通过确定DNA损伤反应来解释大豆(Clycine max(L.)Merr。)对镉毒性的耐受性。
我们的目的是研究调节两个大豆品种对镉的耐受性的DNA错配修复(MMR)基因。在含0-2.5 mg·L-1 Cd的Murashige和Skoog(MS)培养基上,水L生长的辽都10号品种(LD10,对Cd敏感)和神农20(SN20,对镉耐受)。镉胁迫在LD10中引起的随机扩增多态性DNA(RAPD)多态性少于SN20根,导致LD10中的G1 / S阻滞和SN20根中的G2 / M阻滞。LD10-TRV-MLH1幼苗中MLH1的病毒诱导基因沉默(VIGS)显示,镉胁迫下G1 / S阻滞明显减少,但根长/面积增加。然而,SN20-TRV-MSH2和SN20-TRV-MSH6幼苗的G1 / S停滞增加和G2 / M停滞的减少在Cd胁迫下根长/面积减小。综上所述,我们得出的结论是,MSH2和MSH6的低表达,参与G2 / M逮捕,导致Cd诱导的DNA损伤识别绕过MMR系统,借助MLH1激活G1 / S逮捕。然后,这导致LD10的根生长受到抑制,从而解释了大豆对Cd的耐受性的种间差异。