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The synthesis and characterisation (IR, NMR, HR-MS, and X-ray crystallography) of six oxazoline Zn complexes, containing enolate ligands derived from a series of (Z)-1-R-2-(4',4'-dimethyl-2'-oxazolin-2'-yl)-efh-1-en-1-ols (R=[C.sub.6][H.sub.5], [C.sub.6][H.sub.4]-p-N[O.sub.2], [C.sub.6][H.sub.4]-p-O[CH.sub.3], [CF.sub.3], [CH.sub.3], or [CMe.sub.3]) is detailed. All derivatives are air-stable solids of formula Zn[([L.sup.n]).sub.2] and are formed in the presence of the title ligands and [NEt.sub.3]. Reasonable yields (53%-82%) are obtained with the exception of R= [CMe.sub.3] (9%); in this case, by-product formation and high solubility affected complex isolation. Crystallographic characterisation reveals that in all cases the ligands are bound in a [kappa].sup.2]-N, O-bonding motif. Little structural diversity is noted within the series; these complexes are further placed into structural context with related Zn materials containing oxazoline, phenolate, and (or) Schiff base ligands. Key words: oxazoline, coordination complexes, zinc, enolate, X-ray crystal structure, Introduction The naturally occurring Group 12 elements hold a unique position within coordination chemistry due to the overwhelming predominance of the +2 oxidation state. This is, of course, a result [...]

Background: Many specialized cells in adult organs acquire a state of cell cycle arrest and quiescence through unknown mechanisms. Our limited understanding of mammalian cell cycle arrest is derived primarily from cell culture models. Adult mammalian cardiomyocytes, a classic example of cell cycle arrested cells, exit the cell cycle postnatally and remain in an arrested state for the life of the organism. Cardiomyocytes can be induced to re-enter the cell cycle by YAP5SA, an active form of the Hippo signaling pathway effector YAP., Methods: We performed clonal analyses to determine the cell kinetics of YAP5SA cardiomyocytes. We also performed single-cell RNA sequencing, marker gene analysis, and functional studies to examine how YAP5SA cardiomyocytes progress through the cell cycle., Results: We discovered that YAP5SA-expressing cardiomyocytes divided efficiently, with >20% of YAP5SA cardiomyocyte clones containing ≥2 cardiomyocytes. YAP5SA cardiomyocytes re-entered cell cycle at the G1/S transition and had an S phase lasting ≈48 hours. Sarcomere disassembly is required for cardiomyocyte progression from S to G2 phase and the induction of mitotic rounding. Although oscillatory Cdk expression was induced in YAP5SA cardiomyocytes, these cells inefficiently progressed through G2 phase. This is improved by inhibiting P21 function, implicating checkpoint activity as an additional barrier to YAP5SA-induced cardiomyocyte division., Conclusions: Our data reveal that YAP5SA overcomes the mechanically constrained myocardial microenvironment to induce mitotic rounding with cardiomyocyte division, thus providing new insights into the in vivo mechanisms that maintain cell cycle quiescence in adult mammals.