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Coral reef restoration is a rapidly growing movement galvanized by the accelerating degradation of the world's tropical coral reefs. The need for concerted and collaborative action focused on the recovery of coral reef ecosystems coalesced in the creation of the Coral Restoration Consortium (CRC) in 2017. In March 2020, the CRC leadership team met for a biennial review of international coral reef restoration efforts and a discussion of perceived knowledge and implementation bottlenecks that may impair scalability and efficacy. Herein we present six priorities wherein the CRC will foster scientific advancement and collaboration to: (1) increase restoration efficiency, focusing on scale and cost‐effectiveness of deployment; (2) scale up larval‐based coral restoration efforts, emphasizing recruit health, growth, and survival; (3) ensure restoration of threatened coral species proceeds within a population‐genetics management context; (4) support a holistic approach to coral reef ecosystem restoration; (5) develop and promote the use of standardized terms and metrics for coral reef restoration; and (6) support coral reef restoration practitioners working in diverse geographic locations. These priorities are not exhaustive nor do we imply that accomplishing these tasks alone will be sufficient to restore coral reefs globally; rather these are topics where we feel the CRC community of practice can make timely and significant contributions to facilitate the growth of coral reef restoration as a practical conservation strategy. The goal for these collective actions is to provide tangible, local‐scale advancements in reef condition that offset declines resulting from local and global stressors including climate change. [ABSTRACT FROM AUTHOR]

Significant population declines in Acropora cervicornis and A. palmata began in the 1970s and now exceed over 90%. The losses were caused by a combination of coral disease and bleaching, with possible contributions from other stressors, including pollution and predation. Reproduction in the wild by fragment regeneration and sexual recruitment is inadequate to offset population declines. Starting in 2007, the Coral Restoration Foundation™ evaluated the feasibility of outplanting A. cervicornis colonies to reefs in the Florida Keys to restore populations at sites where the species was previously abundant. Reported here are the results of 20 coral outplanting projects with each project defined as a cohort of colonies outplanted at the same time and location. Photogrammetric analysis and in situ monitoring (2007 to 2015) measured survivorship, growth, and condition of 2419 colonies. Survivorship was initially high but generally decreased after two years. Survivorship among projects based on colony counts ranged from 4% to 89% for seven cohorts monitored at least five years. Weibull survival models were used to estimate survivorship beyond the duration of the projects and ranged from approximately 0% to over 35% after five years and 0% to 10% after seven years. Growth rate averaged 10 cm/year during the first two years then plateaued in subsequent years. After four years, approximately one-third of surviving colonies were ≥ 50 cm in maximum diameter. Projects used three to sixteen different genotypes and significant differences did not occur in survivorship, condition, or growth. Restoration times for three reefs were calculated based on NOAA Recovery Plan (NRP) metrics (colony abundance and size) and the findings from projects reported here. Results support NRP conclusions that reducing stressors is required before significant population growth and recovery will occur. Until then, outplanting protects against local extinction and helps to maintain genetic diversity in the wild. [ABSTRACT FROM AUTHOR]

William Hodges 1744-1797 The Art of Exploration Geoff Quilley, Curator Organized by the National Maritime Museum, Greenwich, UK, and the Yale Center for British Art, New Haven, CT. At the [...]

Gene(sis) Contemporary Art Explores Human Genomics Robin Held, curator Organized by the Henry Art Gallery, the University of Washington, Seattle, WA, in affiliation with the Berkeley Art Museum, Berkeley, CA. [...]

Schnyder crystalline corneal dystrophy (SCCD) is a rare autosomal dominant disease characterized by progressive corneal opacification resulting from abnormal deposition of cholesterol and phospholipids. Recently, six different mutations on the UBIAD1 gene on chromosome 1p36 were found to result in SCCD. The purpose of this article is to further characterize the mutation spectrum of SCCD and identify structural and functional consequences for UBIAD1 protein activity. DNA sequencing was performed on samples from 36 individuals from 14 SCCD families. One affected individual was African American and SCCD has not been previously reported in this ethnic group. We identified UBIAD1 mutations in all 14 families which had 30 affected and 6 unaffected individuals. Eight different UBIAD1 mutations, 5 novel (L121F, D118G, and S171P in exon 1, G186R and D236E in exon 2) were identified. In four families with DNA samples from both affected and unaffected individuals, the D118G, G186R, T175I, and G177R mutations cosegregated with SCCD. In combination with our previous report, we have identified the genetic mutation in UBIAD1 in 20 unrelated families with 10 (including 5 reported here), having the N102S mutation. The results suggest that N102S may be a mutation hot spot because the affected families were unrelated including Caucasian and Asian individuals. There was no genotype phenotype correlation except for the T175I mutation which demonstrated prominent diffuse corneal haze, typically without corneal crystals. Protein analysis revealed structural and functional implications of SCCD mutations which may affect UBIAD1 function, ligand binding and interaction with binding partners, like apo E.

Purpose: Schnyder crystalline corneal dystrophy (SCCD; MIM 121800) is a rare autosomal dominant disease characterized by an abnormal increase in cholesterol and phospholipid deposition in the cornea, leading to progressive corneal opacification. Although SCCD has been mapped to a genetic interval between markers D1S1160 and D1S1635, reclassification of a previously unaffected individual expanded the interval to D1S2667 and included nine additional genes. Three candidate genes that may be involved in lipid metabolism and/or are expressed in the cornea were analyzed., Methods: DNA samples were obtained from six families with clinically confirmed SCCD. Analysis of FRAP1, ANGPTL7, and UBIAD1 was performed by PCR-based DNA sequencing, to examine protein-coding regions, RNA splice junctions, and 5' untranslated region (UTR) exons., Results: No disease-causing mutations were found in the FRAP1 or ANGPTL7 gene. A mutation in UBIAD1 was identified in all six families: Five families had the same N102S mutation, and one family had a G177R mutation. Predictions of the protein structure indicated that a prenyl-transferase domain and several transmembrane helices are affected by these mutations. Each mutation cosegregated with the disease in four families with DNA samples from both affected and unaffected individuals. Mutations were not observed in 100 control DNA samples (200 chromosomes)., Conclusions: Nonsynonymous mutations in the UBIAD1 gene were detected in six SCCD families, and a potential mutation hot spot was observed at amino acid N102. The mutations are expected to interfere with the function of the UBIAD1 protein, since they are located in highly conserved and structurally important domains.