ارتباط سطح مقاومت به بیماری آتشک (Erwinia amylovora) با تنش اکسیداتیو کلروپلاستی و میتوکندریائی در دو رقم گلابی هاروسوئیت و بارتلت

نوع مقاله : مقاله پژوهشی

نویسندگان

1 بخش بیوتکنولوژی کشاورزی، واحد علوم تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.

2 پژوهشکده میوه های معتدله وسردسیری، موسسه تحقیقات علوم باغبانی، سازمان تحقیقات، آموزش و ترویج کشاورزی، کرج، ایران.

چکیده

تنش اکسیداتیو ناشی از باکتری بیماری آتشک در گیاه میزبان شامل دو تنش اکسیداتیو کلروپلاستی و میتوکندریائی است و این تنش در نهایت منجر به بروز نکروز در بافت‌ها می‌شود. این پژوهش با هدف مقایسه سهم دو اندامک کلروپلاست و میتوکندری در ایجاد نکروز بیماری با استفاده از بازدارنده زنجیره انتقال الکترون کلروپلاستی گلوتارآلدهید و میتوکندریائی روتنون در دو رقم گلابی ( بارتلت و هاروسوییت) انجام شد. با توجه به تاثیر نکروززائی دو بازدارنده فوق، در آزمایش‌های مقدماتی غلظت بهینه گلوتارآلدهید و روتنون در شرایط درون شیشه تعیین و با توجه به تاثیر یکسان غلظت‌های 5 و 10 میلی‌گرم بر لیتر دو بازدارنده، این غلظت‌ها برای ارزیابی کشت توام باکتری و میزبان مورد استفاده قرار گرفتند. در بررسی اثر متقابل باکتری با ارقام گلابی، ظهور نکروز در رقم حساس بارتلت و متحمل هاروسوئیت به ترتیب 48 و 72 ساعت پس از آلوده‌سازی مشاهده شد. لیکن استفاده از بازدارنده‌ روتنون و گلوتارآلدهید در هر دو غلظت 5 و 10 میلی‌گرم بر لیتر، تاخیر در زمان ظهور اولین علائم و کاهش سرعت پیشرفت نکروز را در هر دو رقم به همراه داشت. در رقم هاروسوئیت، تاثیر بیشتر بازدارنده گلوتارآلدهید در غلظت 10 میلی‌گرم بر لیتر دیده شد. تاثیر بیشتر بازدارنده کلروپلاستی گلوتارآلدهید در شدت بازدارندگی تقریباً یکسان با بازدارنده میتوکندریائی روتنون بیانگر احتمال تاثیر بیشتر زنجیره انتقال الکترون کلروپلاستی در تنش اکسیداتیو حاصل از بیماری آتشک در میزبان بود. علاوه بر این، در رقم حساس بارتلت در شرایط استفاده از بازدارنده‌ میتوکندریائی میزان نزدیکی سرعت پیشرفت علائم نکروز نسبت به شرایط استفاده از بازدارنده کلروپلاستی بیشتر بود که می‌تواند دلیلی بر نقش موثر‌ترکلروپلاست در تحمل به آتشک در رقم متحمل هاروسوئیت باشد.

کلیدواژه‌ها


عنوان مقاله [English]

Association of Resistance Level to the Fire Blight (Erwinia amylovora) Disease with Chloroplastic and Mitochondrial Oxidative Stress in Two Pear Cultivars Harrow Sweet and Barteltt

نویسندگان [English]

  • M. Seyedi 1
  • H. Abdollahi 2
1 Department of Agricultural Biotechnology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
2 Temperate Fruits Research Center, Horticultural Sciences Research Institute, Agricultural Research, Education and Extension Organization, Karaj, Iran.
چکیده [English]

Oxidative stress of the fire blight disease in host plant consists of chloroplastic and mitochondrial oxidative stresses that leads to the necrosis of tissues. This research was conducted to quantify and compare the role of oxidative stress of these organelles using glutaraldehyde as chloroplastic inhibitor of electron transport chain (ETC) and rotenone as mitochondrial inhibitor ETC. Due to the necrotic effect of inhibitors, in the primarily tests, different concentrations of inhibitors were examined under in vitro conditions and two concentrations of inhibitors (5 and 10 mg l-1) were optimized for co-cultivation tests of host-pathogen interaction. In co-cultivation tests, necrosis appearance was recorded at 48 and 72 hours after inoculation in susceptible cv. Bartlett and tolerant cv. Harrow Sweet, respectively. Although both concentrations of inhibitors postponed necrosis appearance and reduced necrosis progress rate, but in cv. Harrow Sweet, higher effects of glutaraldehyde were observed in 10 mg l-1. The higher effects of chloroplastic glutaraldehyde inhibitor demonstrated more effective role of the chloroplastic ETC in oxidative stress of pathogen in comparison with the role of mitochondrial ETC. Additionally, in susceptible cv. Bartlett, mitochondrial inhibitor caused similar necrosis progress rate to the chloroplastic inhibitor which demonstrated another evidence for more effective role of chloroplast organelle in resistance to the fire blight disease in cv. Harrow Sweet.

کلیدواژه‌ها [English]

  • Pear
  • resistance
  • necrosis
  • organelle
  • glutaraldehyde
  • rotenone
  • electron transport chain
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