Resistance of progenies of cacao to Ceratocystis wilt

Resistance of progenies of cacao to Ceratocystis wilt Seedlings from open-pollinated progenies of 20 clones of cocoa (Theobroma cacao) were inoculated with the fungus Ceratocystis cacaofunesta, the causal agent of Ceratocystis wilt, and their response was assessed based on the percentage of dead plants. Open pollinated progeny of clones TSH1188 and VB1151 were used as standards for resistance, while CCN51 and SJ02 for susceptibility. Contrasts between these benchmarks and the progenies studied were estimated and evaluated by Dunnett's t test (alpha = 0.05). The progenies showed different responses to C. cacaofunesta, and it was possible to classify them into three groups: resistant (FCB01, CSG70, BOBA01, VB902, TSH1188, VB1151, PS1319 and MAC01), moderately susceptible (HW25, PM02, FA13, PH15, M05 and BJ11) and susceptible (CCN51, FB206, PH16, SJ02, CCN10 and FSU77).

Enzyme replacement prevents enamel defects in hypophosphatasia mice

Hypophosphatasia (HPP) is the inborn error of metabolism characterized by deficiency of alkaline phosphatase activity, leading to rickets or osteomalacia and to dental defects. HPP occurs from loss-of-function mutations within the gene that encodes the tissue-nonspecific isozyme of alkaline phosphatase (TNAP). TNAP knockout (Alpl-/-, aka Akp2-/-) mice closely phenocopy infantile HPP, including the rickets, vitamin B6-responsive seizures, improper dentin mineralization, and lack of acellular cementum. Here, we report that lack of TNAP in Alpl-/- mice also causes severe enamel defects, which are preventable by enzyme replacement with mineral-targeted TNAP (ENB-0040). Immunohistochemistry was used to map the spatiotemporal expression of TNAP in the tissues of the developing enamel organ of healthy mouse molars and incisors. We found strong, stage-specific expression of TNAP in ameloblasts. In the Alpl-/- mice, histological, mu CT, and scanning electron microscopy analysis showed reduced mineralization and disrupted organization of the rods and inter-rod structures in enamel of both the molars and incisors. All of these abnormalities were prevented in mice receiving from birth daily subcutaneous injections of mineral-targeting, human TNAP at 8.2?mg/kg/day for up to 44 days. These data reveal an important role for TNAP in enamel mineralization and demonstrate the efficacy of mineral-targeted TNAP to prevent enamel defects in HPP. (C) 2012 American Society for Bone and Mineral Research.