ﺷﺒﮑﻪ ﻫﺎي ﺗﻨﻈﯿﻢ ژﻧﯽ ﮐﻨﺘﺮل ﮐﻨﻨﺪه ﻓﺮآﯾﻨﺪﻫﺎي ﮐﺎﺗﺎﺑﻮﻟﯿﮏ ﻣﺘﺎﺑﻮﻟﯿﺴﻢ ﻣﺮﮐﺰي در ﻃﯽ ﭘﯿﺮي و ﮐﺎرﺑﺮد آن در ﺑﻪ نژادي گياهي

Gene regulatory networks governing catabolic processes of central metabolism during senescence and its application in plant breeding

ﭘﯿﺮي آﺧﺮﯾﻦ ﻣﺮﺣﻠﻪ ﻧﻤﻮي ﺑﺮگ اﺳﺖ ﮐﻪ ﻃﯽ آن ﻣﺎﮐﺮوﻣﻮﻟﮑﻮﻟﻬﺎ در ﻣﻌﺮض ﻓﺮآﯾﻨﺪﻫﺎي ﺗﺠﺰﯾﻪاي ﻗﺮار ﮔﺮﻓﺘﻪ ﺗﺎ ﻣﻮاد ﻣﻐﺬي در ﺑﺮگ ﻣﺴﻦ ﺑﺎزﯾﺎﻓﺖ ﺷﺪه و ﺑﻪ ﺑﺬور در ﺣﺎل ﻧﻤﻮ اﻧﺘﻘﺎل ﯾﺎﺑﻨﺪ. ﻟﺬا ﭘﯿﺮي ﺑﺎ ﺗﻐﯿﯿﺮات ﻋﻤﺪه در ﻣﺘﺎﺑﻮﻟﯿﺴﻢ ﻣﺮﮐﺰي ﮔﯿﺎه ﺻﻮرت ﻣﯽﭘﺬﯾﺮد. ﻣﺎ ﺑﺎ ﺑﻬﺮهﮔﯿﺮي از ﻣﺘﺪﻫﺎي زﯾﺴﺖ ﺷﻨﺎﺳﯽ ﻣﻮﻟﮑﻮﻟﯽ، ژﻧﺘﯿﮑﯽ، ﺑﯿﻮﺷﯿﻤﯿﺎﯾﯽ و ﻣﺘﺎﺑﻮﻟﯿﮑﯽ ﻣﺸﺨﺺ ﻧﻤﻮدﯾﻢ ﮐﻪ ﻋﺎﻣﻞ روﻧﻮﯾﺴﯽ RD26 ازﺧﺎﻧﻮاده NAC ﯾﮏ ﺗﻨﻈﯿﻢ ﮐﻨﻨﺪه اﺻﻠﯽ ﺑﺎزآراﯾﯽ ﮔﺴﺘﺮده در ﺑﺮﻧﺎﻣﻪﻫﺎي ﻣﺘﺎﺑﻮﻟﯿﮑﯽ ﻣﺮﮐﺰي ﮔﯿﺎه در ﻃﯽ ﭘﯿﺮي و ﺗﻨﺶ اﺳﺖ. دادهﻫﺎي ﻣﺎ ﻣﺸﺨﺺ ﻧﻤﻮدﻧﺪ ﮐﻪ RD26 ﺗﻨﻈﯿﻢ ﮐﻨﻨﺪه ﻣﺜﺒﺖ ﭘﯿﺮي و ﭘﺎﺳﺦ ﺑﻪ ﺗﻨﺶ اﺳﺖ. RD26 ﺑﻪ ﻃﻮر ﻣﺴﺘﻘﯿﻢ ﺑﺮ ﭘﺮوﻣﻮﺗﺮ ژﻧﻬﺎيCV وClpD ﻧﺸﺴﺘﻪ و اﻟﻘﺎي ﺑﯿﺎن آﻧﻬﺎ را ﻣﻨﺠﺮ ﺷﺪه و از ﻃﺮﯾﻖ آﻧﻬﺎ ﺗﺠﺰﯾﻪ ﭘﺮوﺗﺌﯿﻨﻬﺎي ﮐﻠﺮوﭘﻼﺳﺘﯽ در ﺧﻼل ﭘﯿﺮي را ﻣﯽاﻧﮕﯿﺰد. RD26 ﻫﻤﭽﻨﯿﻦ ﺑﺎ اﻟﻘﺎي ﻣﺴﺘﻘﯿﻢ ﺑﯿﺎن ژن LKR/SDH وPES1 ﺑﻪ ﺗﺮﺗﯿﺐ ﺗﺠﺰﯾﻪ اﻣﯿﻨﻮ اﺳﯿﺪ ﻻﯾﺴﯿﻦ و زﻧﺠﯿﺮه ﺣﺪواﺳﻂ ﻓﺎﯾﺘﻮل را ﻓﻌﺎل ﻣﯽﺳﺎزد. ﻫﻤﯿﻦ ﻃﻮر RD26 ﺗﺠﺰﯾﻪ ﮔﺎﺑﺎ راﻣﯽاﻧﮕﯿﺰاﻧﺪ. ﻫﺮ ﺳﻪ ﻣﺴﯿﺮ ﻓﻮق ﺑﺎ ﺗﺎﻣﯿﻦ ﭘﯿﺶ ﻣﺎدهﻫﺎي آﻟﺘﺮﻧﺎﺗﯿﻮ در ﺷﺮاﯾﻂ ﮔﺮﺳﻨﮕﯽ ﮐﺮﺑﻨﯽ، ﺗﻨﻔﺲ ﻣﺎﯾﺘﻮﮐﻨﺪرﯾﺎﯾﯽ و ﺗﺎﻣﯿﻦ اﻧﺮژي ﺑﺮاي اﻧﺘﻘﺎل ﻣﻮاد را ﻣﻤﮑﻦ ﻣﯽﺳﺎزﻧﺪ. RD26 ﻫﻤﭽﻨﯿﻦ ﺑﺎ اﻟﻘﺎي ﻣﺴﺘﻘﯿﻢ ژﻧﻬﺎي AMY1، SWEET15 و SFP1 ﺗﺠﺰﯾﻪ ﻧﺸﺎﺳﺘﻪ و ﺗﺠﻤﻊ واﻧﺘﻘﺎل ﻗﻨﺪﻫﺎي ﺳﺎده را اﻟﻘﺎ ﻧﻤﻮد. ﺷﻨﺎﺧﺖ ﭼﮕﻮﻧﮕﯽ ﺗﻨﻈﯿﻢ ﻣﻮﻟﮑﻮﻟﯽ ﺗﻐﯿﯿﺮات ﻋﻤﺪه ﻣﺘﺎﺑﻮﻟﯿﮑﯽ در ﻃﯽ ﭘﯿﺮي و ﺗﻨﺶ در ﺗﻮﻟﯿﺪ ارﻗﺎم ﺑﺎ ﻃﻮل ﻋﻤﺮ ﻣﺘﻔﺎوت، ﺑﻬﺒﻮد ﺷﺮاﯾﻂ ﭘﺲ از ﺑﺮداﺷﺖ، اﻓﺰاﯾﺶ ارزش ﺗﻐﺬﯾﻪاي ﻣﺤﺼﻮل، ﻣﻬﻨﺪﺳﯽ ﻣﺘﺎﺑﻮﻟﯿﮑﯽ ارﻗﺎم ﺑﺎ ﻫﺪف ﻣﺼﺮف ﺧﺎص و ﺑﻬﺒﻮد ﮐﺎراﯾﯽ ﻣﺼﺮف ﻣﻮادﻣﻐﺬي ﮔﯿﺎه ﺑﺴﯿﺎر راﻫﮕﺸﺎ ﺧﻮاﻫﺪ ﺑﻮد.

Leaf senescence is a key process in plants that culminates in the degradation of cellular constituents and massive reprogramming of metabolism for the recovery of nutrients from aged leaves for their reuse in newly developing sinks. We employed molecular-biological and metabolomics approaches to identify NAC transcription factor TF RD26 as a master regulator of metabolic reprogramming in Arabidopsis thaliana. RD26 directly activates CHLOROPLAST VESICULATION CV, a protein crucial for chloroplast protein degradation, concomitant with an enhanced protein loss in RD26 overexpressors during senescence, but a reduced decline of protein in rd26 knockout mutants. RD26 also directly activates LKR/SDH involved in lysine catabolism, and PES1 important for phytol degradation. Metabolic profiling revealed reduced γ-amino butyric acid GABA in RD26 overexpressors, accompanied by the induction of respective catabolic genes. Degradation of lysine, phytol and GABA is instrumental for maintaining mitochondrial respiration in carbon-limiting conditions during senescence. RD26 also supports the degradation of starch and the accumulation of mono- and disaccharides during senescence by directly enhancing the expression of AMY1, SFP1 and SWEET15 involved in carbohydrate metabolism and transport. Collectively, during senescence RD26 acts by controlling the expression of genes across the entire spectrum of the cellular degradation hierarchy.