Louis Pasteur first reported that living cells switch from aerobic to anaerobic metabolism under low-oxygen conditions,but the underlying regulatory mechanism remains to be fully elucidated.ALCOHOL DEHYDROGENASE 1(ADH...Louis Pasteur first reported that living cells switch from aerobic to anaerobic metabolism under low-oxygen conditions,but the underlying regulatory mechanism remains to be fully elucidated.ALCOHOL DEHYDROGENASE 1(ADH1)encodes a key enzyme in ethanolic fermentation and is upregulated under hypoxia.In this study,we searched for Arabidopsis thaliana mutants with defects in hypoxia-induced ADH1 expression and identified the IQ DOMAIN containing protein 22(IQD22)as a crucial regulator of ADH1-mediated hypoxia tolerance.The iqd22 mutant plants were hypersensitive to submergence and hypoxic stress as compared with the wild-type plants,whereas IQD22 overexpressors were more tolerant.We showed that under hypoxia,IQD22 enhances the interaction between the calcium-dependent protein kinase CPK12 and the ETHYLENE RESPONSE FACTOR(ERF)-VII-type transcription factor RELATED TO AP2.12(RAP2.12)to upregulate hypoxia-responsive genes,including ADH1.Moreover,we found that IQD22 interacts with calmodulins(CaMs)in vivo and facilitates their association with ADH1,stimulating its abundance in response to hypoxia.Metabolic profiling revealed that hypoxia causes significant increase in glycolytic metabolites but greatly lower ethanol accumulation in the iqd22-2 mutant.Genetic analysis showed that disruption of ADH1 suppresses the improved hypoxia-tolerance phenotype of IQD22 overexpressors.Taken together,these results indicate that IQD22 functions in the CaM-ADH1 and CPK12-RAP2.12 regulatory modules,which coordinately mediate calcium-dependent activation of anaerobic respiration to control metabolic flux during hypoxia.展开更多
In plants, cortical microtubules anchor to the plasma membrane in arrays and play important roles in cell shape. However, the molecular mechanism of microtubule binding proteins, which connect the plasma membrane and ...In plants, cortical microtubules anchor to the plasma membrane in arrays and play important roles in cell shape. However, the molecular mechanism of microtubule binding proteins, which connect the plasma membrane and cortical microtubules in cell morphology remains largely unknown. Here, we report that a plasma membrane and microtubule duallocalized IQ67 domain protein, IQD21, is critical for cotyledon pavement cell(PC) morphogenesis in Arabidopsis. iqd21 mutation caused increased indentation width, decreased lobe length, and similar lobe number of PCs, whereas IQD21 overexpression had a different effect on cotyledon PC shape. Weak overexpression led to increased lobe number, decreased indentation width, and similar lobe length, while moderate or great overexpression resulted in decreased lobe number, indentation width, and lobe length of PCs. Live-cell observations revealed that IQD21 accumulation at indentation regions correlates with lobe initiation and outgrowth during PC development. Cell biological and genetic approaches revealed that IQD21 promotes transfacial microtubules anchoring to the plasma membrane via its polybasic sites and bundling at the indentation regions in both periclinal and anticlinal walls. IQD21 controls cortical microtubule organization mainly through promoting Katanin 1-mediated microtubule severing during PC interdigitation. These findings provide the genetic evidence that transfacial microtubule arrays play a determinant role in lobe formation, and the insight into the molecular mechanism of IQD21 in transfacial microtubule organization at indentations and puzzle-shaped PC development.展开更多
基金supported by the National Key R&D Program of China(Project 2024YFD1200800)the National Natural Science Foundation of China(pProjects 32321163646,U22A20458,and 32202468)the Natural Science Foundation of Guangdong Province(pProjects 2023A1515012038).
文摘Louis Pasteur first reported that living cells switch from aerobic to anaerobic metabolism under low-oxygen conditions,but the underlying regulatory mechanism remains to be fully elucidated.ALCOHOL DEHYDROGENASE 1(ADH1)encodes a key enzyme in ethanolic fermentation and is upregulated under hypoxia.In this study,we searched for Arabidopsis thaliana mutants with defects in hypoxia-induced ADH1 expression and identified the IQ DOMAIN containing protein 22(IQD22)as a crucial regulator of ADH1-mediated hypoxia tolerance.The iqd22 mutant plants were hypersensitive to submergence and hypoxic stress as compared with the wild-type plants,whereas IQD22 overexpressors were more tolerant.We showed that under hypoxia,IQD22 enhances the interaction between the calcium-dependent protein kinase CPK12 and the ETHYLENE RESPONSE FACTOR(ERF)-VII-type transcription factor RELATED TO AP2.12(RAP2.12)to upregulate hypoxia-responsive genes,including ADH1.Moreover,we found that IQD22 interacts with calmodulins(CaMs)in vivo and facilitates their association with ADH1,stimulating its abundance in response to hypoxia.Metabolic profiling revealed that hypoxia causes significant increase in glycolytic metabolites but greatly lower ethanol accumulation in the iqd22-2 mutant.Genetic analysis showed that disruption of ADH1 suppresses the improved hypoxia-tolerance phenotype of IQD22 overexpressors.Taken together,these results indicate that IQD22 functions in the CaM-ADH1 and CPK12-RAP2.12 regulatory modules,which coordinately mediate calcium-dependent activation of anaerobic respiration to control metabolic flux during hypoxia.
基金supported by funding from the National Natural Science Foundation of China (31970730, 32170721)。
文摘In plants, cortical microtubules anchor to the plasma membrane in arrays and play important roles in cell shape. However, the molecular mechanism of microtubule binding proteins, which connect the plasma membrane and cortical microtubules in cell morphology remains largely unknown. Here, we report that a plasma membrane and microtubule duallocalized IQ67 domain protein, IQD21, is critical for cotyledon pavement cell(PC) morphogenesis in Arabidopsis. iqd21 mutation caused increased indentation width, decreased lobe length, and similar lobe number of PCs, whereas IQD21 overexpression had a different effect on cotyledon PC shape. Weak overexpression led to increased lobe number, decreased indentation width, and similar lobe length, while moderate or great overexpression resulted in decreased lobe number, indentation width, and lobe length of PCs. Live-cell observations revealed that IQD21 accumulation at indentation regions correlates with lobe initiation and outgrowth during PC development. Cell biological and genetic approaches revealed that IQD21 promotes transfacial microtubules anchoring to the plasma membrane via its polybasic sites and bundling at the indentation regions in both periclinal and anticlinal walls. IQD21 controls cortical microtubule organization mainly through promoting Katanin 1-mediated microtubule severing during PC interdigitation. These findings provide the genetic evidence that transfacial microtubule arrays play a determinant role in lobe formation, and the insight into the molecular mechanism of IQD21 in transfacial microtubule organization at indentations and puzzle-shaped PC development.
