Kumar G N Mohan, Iyer Suresh, Knowles N Richard
Postharvest Physiology and Biochemistry Laboratory, Department of Horticulture and Landscape Architecture, Washington State University, Pullman, WA 99164-6414, USA.
Planta. 2007 Dec;227(1):25-36. doi: 10.1007/s00425-007-0589-9. Epub 2007 Jul 26.
During 30-months of storage at 4 degrees C, potato (Solanum tuberosum L.) tubers progressively lose the ability to produce superoxide in response to wounding, resist microbial infection, and develop a suberized wound periderm. Using differentially aged tubers, we demonstrate that Strboh A is responsible for the wound-induced oxidative burst in potato and aging attenuates its expression. In vivo superoxide production and NADPH oxidase (NOX) activity from 1-month-old tubers increased to a maximum 18-24 h after wounding and then decreased to barely detectable levels by 72 h. Wounding also induced a 68% increase in microsomal protein within 18 h. These wound-induced responses were lost over a 25- to 30-month storage period. Superoxide production and NOX activity were inhibited by diphenylene iodonium chloride, a specific inhibitor of NOX, which in turn effectively inhibited wound-healing and increased susceptibility to microbial infection and decay in 1-month-old tubers. Wound-induced superoxide production was also inhibited by EGTA-mediated destabilization of membranes. The ability to restore superoxide production to EGTA-treated tissue with Ca(+2) declined with advancing tuber age, likely a consequence of age-related changes in membrane architecture. Of the five homologues of NOX (Strboh A-D and F), wounding induced the expression of Strboh A in 6-month-old tubers but this response was absent in tubers stored for 25-30 months. Strboh A thus mediates the initial burst of superoxide in response to wounding of potato tubers; loss of its expression increases the susceptibility to microbial infection and contributes to the age-induced loss of wound-healing ability.
在4℃下储存30个月期间，马铃薯（Solanum tuberosum L.）块茎对伤口产生超氧化物的能力、抵抗微生物感染的能力以及形成木栓化伤口周皮的能力会逐渐丧失。使用不同年龄的块茎，我们证明Strboh A负责马铃薯伤口诱导的氧化爆发，并且衰老会减弱其表达。1月龄块茎的体内超氧化物产生和NADPH氧化酶（NOX）活性在受伤后18 - 24小时增加到最大值，然后在72小时时降至几乎检测不到的水平。受伤还会在18小时内使微粒体蛋白增加68%。这些伤口诱导的反应在25至30个月的储存期内会消失。二苯基碘鎓氯化物是NOX的特异性抑制剂，它抑制了超氧化物的产生和NOX活性，进而有效抑制了1月龄块茎的伤口愈合，并增加了其对微生物感染和腐烂的易感性。EGTA介导的膜去稳定作用也抑制了伤口诱导的超氧化物产生。用Ca(+2)将超氧化物产生恢复到EGTA处理组织的能力随着块茎年龄的增长而下降，这可能是膜结构与年龄相关变化的结果。在NOX的五个同源物（Strboh A - D和F）中，受伤诱导6月龄块茎中Strboh A的表达，但在储存25 - 30个月的块茎中这种反应不存在。因此，Strboh A介导了马铃薯块茎受伤时超氧化物的初始爆发；其表达的丧失增加了对微生物感染的易感性，并导致了与年龄相关的伤口愈合能力丧失。
