The P_(S) defect is obtained by replacing one S atom with one P atom in the wide-bandgap semiconductor Mg S.Based on first-principles calculations,the formation energy,defect levels,and electronic structure of the PSd...The P_(S) defect is obtained by replacing one S atom with one P atom in the wide-bandgap semiconductor Mg S.Based on first-principles calculations,the formation energy,defect levels,and electronic structure of the PSdefect in different charge states are evaluated.We predict that the neutral P^(0)_(S)and positively charged P^(+1)_(S)are the plausible qubit candidates for the construction of quantum systems,since they maintain the spin conservation during optical excited transition.The zero-phonon lines at the P^(0)_(S)and P^(+1)_(S)defects are 0.43 e V and 0.21 e V,respectively,which fall in the infrared band.In addition,the zero-field splitting parameter D of the P^(+1)_(S)with spin-triplet is 2920 MHz,which is in the range of microwave,showing that the P^(+1)_(S)defect can be manipulated by microwave.Finally,the principal values of the hyperfine tensor are examined,it is found that they decay exponentially with the distance from the defect site.展开更多
Ca^(2+) signaling is critical for heart development;however,the precise roles and regulatory pathways of Ca^(2+) transport proteins in cardiogenesis remain largely unknown.Sodium-calcium exchanger 1(Ncx1)is responsibl...Ca^(2+) signaling is critical for heart development;however,the precise roles and regulatory pathways of Ca^(2+) transport proteins in cardiogenesis remain largely unknown.Sodium-calcium exchanger 1(Ncx1)is responsible for Ca^(2+) efflux in cardiomyocytes.It is involved in cardiogenesis,while the mechanism is unclear.Here,using the forward genetic screening in zebrafish,we identified a novel mutation at a highly-conserved leucine residue in ncx1 gene(mutant^(LDD353)/ncx1h^(L154P))that led to smaller hearts with reduced heart rate and weak contraction.Mechanistically,the number of ventricular but not atrial cardiomyocytes was reduced in ncx1h^(L154P) zebrafish.These defects were mimicked by knockdown or knockout of ncx1h.Moreover,ncx1h^(L154P) had cytosolic and mitochondrial Ca^(2+) overloading and Ca^(2+) transient suppression in cardiomyocytes.Furthermore,ncx1h^(L154P) and ncx1h morphants downregulated cardiac transcription factors hand2 and gata4 in the cardiac regions,while overexpression of hand2 and gata4 partially rescued cardiac defects including the number of ventricular myocytes.These findings demonstrate an essential role of the novel 154th leucine residue in the maintenance of Ncx1 function in zebrafish,and reveal previous unrecognized critical roles of the 154th leucine residue and Ncx1 in the formation of ventricular cardiomyocytes by at least partially regulating the expression levels of gata4 and hand2.展开更多
基金Project supported by the National Natural Science Foundation of China(Grant No.12164020)the Natural Science Foundation of Jiangxi Province,China(Grant No.20202BAB201012)。
文摘The P_(S) defect is obtained by replacing one S atom with one P atom in the wide-bandgap semiconductor Mg S.Based on first-principles calculations,the formation energy,defect levels,and electronic structure of the PSdefect in different charge states are evaluated.We predict that the neutral P^(0)_(S)and positively charged P^(+1)_(S)are the plausible qubit candidates for the construction of quantum systems,since they maintain the spin conservation during optical excited transition.The zero-phonon lines at the P^(0)_(S)and P^(+1)_(S)defects are 0.43 e V and 0.21 e V,respectively,which fall in the infrared band.In addition,the zero-field splitting parameter D of the P^(+1)_(S)with spin-triplet is 2920 MHz,which is in the range of microwave,showing that the P^(+1)_(S)defect can be manipulated by microwave.Finally,the principal values of the hyperfine tensor are examined,it is found that they decay exponentially with the distance from the defect site.
基金supported by grants from the National Natural Science Foundation of China(81520108004,81470422)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDA16010201)+1 种基金National Key R&D Program of China(2017YFA 0103700,2016YFC1301204)to H.-T.Y.Shanghai Natural Science Foundation(17ZR1435500)to J.H。
文摘Ca^(2+) signaling is critical for heart development;however,the precise roles and regulatory pathways of Ca^(2+) transport proteins in cardiogenesis remain largely unknown.Sodium-calcium exchanger 1(Ncx1)is responsible for Ca^(2+) efflux in cardiomyocytes.It is involved in cardiogenesis,while the mechanism is unclear.Here,using the forward genetic screening in zebrafish,we identified a novel mutation at a highly-conserved leucine residue in ncx1 gene(mutant^(LDD353)/ncx1h^(L154P))that led to smaller hearts with reduced heart rate and weak contraction.Mechanistically,the number of ventricular but not atrial cardiomyocytes was reduced in ncx1h^(L154P) zebrafish.These defects were mimicked by knockdown or knockout of ncx1h.Moreover,ncx1h^(L154P) had cytosolic and mitochondrial Ca^(2+) overloading and Ca^(2+) transient suppression in cardiomyocytes.Furthermore,ncx1h^(L154P) and ncx1h morphants downregulated cardiac transcription factors hand2 and gata4 in the cardiac regions,while overexpression of hand2 and gata4 partially rescued cardiac defects including the number of ventricular myocytes.These findings demonstrate an essential role of the novel 154th leucine residue in the maintenance of Ncx1 function in zebrafish,and reveal previous unrecognized critical roles of the 154th leucine residue and Ncx1 in the formation of ventricular cardiomyocytes by at least partially regulating the expression levels of gata4 and hand2.
基金This study was supported by grants from the National Natural Science Foundation of China (31030050, 81520108004, and 81470422 to H.-T.Y.), the Strategic Priority Research Program of Chinese Academy of Sciences (XDA01020204 to H.-T.Y.), the National Basic Research Program of China (2014CB965100 to H.-T.Y.), the National Science and Technology Major Project (2012ZX09501001 to H.-T.Y.), and the Shenzhen Science, Technology and Innovation Committee OCYI 20160428154108239 to K.O.).