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      Permanent link:
      https://www.ias.ac.in/article/fulltext/jgen/096/02/0261-0271

    • Keywords

       

      autoimmune; chlorenchyma; hypersensitive response; posttranslational behaviour; rbcS; rbcL.

    • Abstract

       

      Wheat hybrid necrosis is caused by the interaction of two dominant complementary genes, Ne1 and Ne2, located on chromosome arms 5BL and 2BS, respectively. The sequences of Ne1 or Ne2 have not yet been identified. It is also not known whether Ne1 and Ne2 are structural or regulatory genes. Understanding the proteomic pathways may provide a knowledge base for protecting or maximizing the photosynthesis capacity of wheat. Using DIGE and MALDITOF-TOF MS, the flag leaf protein patterns of the two unique F14 near-isogenic line siblings (NILs), the necrotic ShunMai 12Ah (Ne1Ne1Ne2Ne2) and the normal ShunMai 12Af (Ne1Ne1ne2ne2) were compared. Due to the presence or absence of Ne2, (i) three protein spots were expressed or disappeared, (ii) seven RuBisCO-related proteins were altered significantly, and (iii) 21 photosynthesis/glucose related proteins were changed significantly. Three hypotheses were deduced, (i) Ne1 may also encode protein(s), (ii) genetic maladjustment of RuBisCO could lead to early leaf death, and (iii) interactions between nuclear genes and chloroplast genes could determine photosynthetic traits. Our hypothetical model presents the RuBisCO pathway of hybrid necrosis in wheat and explains how Ne1 and Ne2 interact at molecular level.

    • Author Affiliations

       

      SI RUI PAN1 XING LAI PAN2 QIANYING PAN3 YIN HONG SHI2 LI ZHANG2 YUN FAN2 YAN RUI XUE2

      1. Life Science and Technology A1201, Beijing University of Chemical Technology, Beijing 102200, People’s Republic of China
      2. Department of Food Crop Science, Cotton Research Institute, Shanxi Agriculture Science Academy, Yuncheng, Shanxi 044000, People’s Republic of China
      3. Foreign Language College, Anhui University of Technology and Science, Wuhu, Anhui 241000, People’s Republic of China
    • Dates

       

© 2017 Indian Academy of Sciences, Bengaluru.