Ralstonia solanacearum causes a lethal bacterial wilt disease in many crops,leading to huge losses in crop production every year.Understanding of plant-R.solanacearum interactions will aid to develop efficient strateg...Ralstonia solanacearum causes a lethal bacterial wilt disease in many crops,leading to huge losses in crop production every year.Understanding of plant-R.solanacearum interactions will aid to develop efficient strategies to control the disease.As a soilborne pathogen,R.solanacearum naturally infects plants via roots.A huge limitation in studying plant-R.solanacearum interactions is the large variation of R.solanacearum infection assay due to the variable soil conditions and uneven inoculum exposure.Here,we developed a robust and reliable Petri-dish inoculation method which allows consistent and stable infection in young plant seedlings.This method is easy to use,takes about only 10 days from seed germination to the completion of inoculation assay,and requires less inoculum of bacteria as well as growth chamber space.We proved the efficacy of the seedling Petri-dish inoculation method by analyzing plant defense primed by molecular patterns,resistance of defense-related plant mutants,and virulence of R.solanacearum mutants.Furthermore,we demonstrated that the seedling Petri-dish inoculation method can be applied to other host plants such as tobacco and has great potential for high-throughput screening of resistant plant germplasms to bacterial wilt in the future.展开更多
Pathological cardiac hypertrophy is a maladaptive response in a variety of organic heart disease(OHD),which is characterized by mitochondrial dysfunction that results from disturbed energy metabolism.SIRT3,a mitochond...Pathological cardiac hypertrophy is a maladaptive response in a variety of organic heart disease(OHD),which is characterized by mitochondrial dysfunction that results from disturbed energy metabolism.SIRT3,a mitochondria-localized sirtuin,regulates global mitochondrial lysine acetylation and preserves mitochondrial function.However,the mechanisms by which SIRT3 regulates cardiac hypertrophy remains to be further elucidated.In this study,we firstly demonstrated that expression of SIRT3 was decreased in AngiotensionⅡ(AngⅡ)-treated cardiomyocytes and in hearts of AngⅡ-induced cardiac hypertrophic mice.In addition,SIRT3 overexpression protected myocytes from hypertrophy,whereas SIRT3 silencing exacerbated AngⅡ-induced cardiomyocyte hypertrophy.In particular,SIRT3-KO mice exhibited significant cardiac hypertrophy.Mechanistically,we identified NMNAT3(nicotinamide mononucleotide adenylyltransferase 3),the rate-limiting enzyme for mitochondrial NAD biosynthesis,as a new target and binding partner of SIRT3.Specifically,SIRT3 physically interacts with and deacetylates NMNAT3,thereby enhancing the enzyme activity of NMNAT3 and contributing to SIRT3-mediated anti-hypertrophic effects.Moreover,NMNAT3 regulates the activity of SIRT3 via synthesis of mitochondria NAD.Taken together,these findings provide mechanistic insights into the negative regulatory role of SIRT3 in cardiac hypertrophy.Sirtuin 3(SIRT3),a mitochondrial deacetylase that may play an important role in regulating cardiac function and a potential target for CHF.展开更多
基金This work was supported by the National Natural Science Foundation of China(32072399 and 32272641)the Fundamental Research Funds for the Central Universities(GK202201017 and GK202207024)the Program of Fujian Key Laboratory for Monitoring and Integrated Management of Crop Pests,China(MIMCP-202203).
文摘Ralstonia solanacearum causes a lethal bacterial wilt disease in many crops,leading to huge losses in crop production every year.Understanding of plant-R.solanacearum interactions will aid to develop efficient strategies to control the disease.As a soilborne pathogen,R.solanacearum naturally infects plants via roots.A huge limitation in studying plant-R.solanacearum interactions is the large variation of R.solanacearum infection assay due to the variable soil conditions and uneven inoculum exposure.Here,we developed a robust and reliable Petri-dish inoculation method which allows consistent and stable infection in young plant seedlings.This method is easy to use,takes about only 10 days from seed germination to the completion of inoculation assay,and requires less inoculum of bacteria as well as growth chamber space.We proved the efficacy of the seedling Petri-dish inoculation method by analyzing plant defense primed by molecular patterns,resistance of defense-related plant mutants,and virulence of R.solanacearum mutants.Furthermore,we demonstrated that the seedling Petri-dish inoculation method can be applied to other host plants such as tobacco and has great potential for high-throughput screening of resistant plant germplasms to bacterial wilt in the future.
基金This work was supported by grants from the National Natural Science Foundation of China(No.81673433,No.81026548 and No.81273499),Team item of the Natural Science Foundation of Guangdong Province(No.S2011030003190).
文摘Pathological cardiac hypertrophy is a maladaptive response in a variety of organic heart disease(OHD),which is characterized by mitochondrial dysfunction that results from disturbed energy metabolism.SIRT3,a mitochondria-localized sirtuin,regulates global mitochondrial lysine acetylation and preserves mitochondrial function.However,the mechanisms by which SIRT3 regulates cardiac hypertrophy remains to be further elucidated.In this study,we firstly demonstrated that expression of SIRT3 was decreased in AngiotensionⅡ(AngⅡ)-treated cardiomyocytes and in hearts of AngⅡ-induced cardiac hypertrophic mice.In addition,SIRT3 overexpression protected myocytes from hypertrophy,whereas SIRT3 silencing exacerbated AngⅡ-induced cardiomyocyte hypertrophy.In particular,SIRT3-KO mice exhibited significant cardiac hypertrophy.Mechanistically,we identified NMNAT3(nicotinamide mononucleotide adenylyltransferase 3),the rate-limiting enzyme for mitochondrial NAD biosynthesis,as a new target and binding partner of SIRT3.Specifically,SIRT3 physically interacts with and deacetylates NMNAT3,thereby enhancing the enzyme activity of NMNAT3 and contributing to SIRT3-mediated anti-hypertrophic effects.Moreover,NMNAT3 regulates the activity of SIRT3 via synthesis of mitochondria NAD.Taken together,these findings provide mechanistic insights into the negative regulatory role of SIRT3 in cardiac hypertrophy.Sirtuin 3(SIRT3),a mitochondrial deacetylase that may play an important role in regulating cardiac function and a potential target for CHF.
