ABSTRACT
The first layer of defense that plants deploy to ward off a microbial invasion comes in the form of pattern-triggered immunity (PTI), which is initiated when the pattern-recognition receptors (PRRs) bind with the pathogen-associated molecular patterns (PAMPs) and co-receptor proteins, and transmit a defense signal. Although several plant PRRs have been discovered, very few of them have been fully characterized, and their functional parameters assessed. In this study, the 3D-model prediction of an entire plant PRR protein, Xa21, was done by implementing multiple in silico modeling techniques. Subsequently, the PAMP RaxX21-sY (sulphated RaxX21) and leucine-rich repeat (LRR) domain of the co-receptor OsSERK2 were docked with the LRR domain of Xa21. The docked complex of these three proteins formed a heterodimer that closely resembles the other crystallographic PTI complexes available. Molecular dynamics simulations and MM/PBSA calculations were applied for an in-depth analysis of the interactions between Xa21 LRR, RaxX21-sY, and OsSERK2 LRR. Arg230 and Arg185 from Xa21 LRR, Val2 and Lys15 from RaxX21-sY and Lys164 from OsSERK2 LRR were found to be the prominent residues which might contribute significantly in the formation of a heterodimer during the PTI process mediated by Xa21. Additionally, RaxX21-sY interacted much more favorably with Xa21 LRR in the presence of OsSERK2 LRR in the complex, which substantiates the necessity of the co-receptor in Xa21 mediated PTI to recognize the PAMP RaxX21-sY. However, the free energy binding calculation reveals the favorability of a heterodimer formation of PRR Xa21 and co-receptor OsSERK2 without the presence of PAMP RaxX21-sY, which validate the previous lab result.
ABSTRACT
Time-resolved IR (TRIR) studies on (η(5)-C(5)H(4)Me)Mn(L)(CO) (L = 1,3-diethyl-4,5-dimethylimidazol-2-ylidene, PPh(3)) indicate that the rate of reaction with CO is ca. 10(2) slower for the N-heterocyclic carbene intermediate, which DFT calculations suggest is due to the presence of a strong MnH-C agostic bond. The reactivity of these intermediates in alkane solvents is governed by such interactions rather than solvent coordination to the unsaturated metal centre.
ABSTRACT
A combination of experimental studies and density functional theory calculations is used to study C-N bond activation in a series of ruthenium N-alkyl-substituted heterocyclic carbene (NHC) complexes. These show that prior C-H activation of the NHC ligand renders the system susceptible to irreversible C-N activation. In the presence of a source of HCl, C-H activated Ru(I(i)Pr(2)Me(2))'(PPh(3))(2)(CO)H (1, I(i)Pr(2)Me(2) = 1,3-diisopropyl-4,5-dimethylimidazol-2-ylidene) reacts to give Ru(I(i)PrHMe(2))(PPh(3))(2)(CO)HCl (2, I(i)PrHMe(2) = 1-isopropyl-4,5-dimethylimidazol-2-ylidene) and propene. The mechanism involves (i) isomerization to a trans-phosphine isomer, 1c, in which hydride is trans to the metalated alkyl arm, (ii) C-N cleavage to give an intermediate propene complex with a C2-metalated imidazole ligand, and (iii) N-protonation and propene/Cl(-) substitution to give 2. The overall computed activation barrier (ΔE(++)(calcd)) corresponds to the isomerization/C-N cleavage process and has a value of +24.4 kcal/mol. C-N activation in 1c is promoted by the relief of electronic strain arising from the trans disposition of the high-trans-influence hydride and alkyl ligands. Experimental studies on analogues of 1 with different C4/C5 carbene backbone substituents (Ru(I(i)Pr(2)Ph(2))'(PPh(3))(2)(CO)H, Ru(I(i)Pr(2))'(PPh(3))(2)(CO)H) or different N-substituents (Ru(IEt(2)Me(2))'(PPh(3))(2)(CO)H) reveal that Ph substituents promote C-N activation. Calculations confirm that Ru(I(i)Pr(2)Ph(2))'(PPh(3))(2)(CO)H undergoes isomerization/C-N bond cleavage with a low barrier of only +21.4 kcal/mol. Larger N-alkyl groups also facilitate C-N bond activation (Ru(I(t)Bu(2)Me(2))'(PPh(3))(2)(CO)H, ΔE(++)(calcd) = +21.3 kcal/mol), and in this case the reaction is promoted by the formation of the more highly substituted 2-methylpropene.
