Successive bleaching events cause mass coral mortality in Guam, Micronesia

The reefs of Guam, a high island in the Western Pacific, were impacted by an unprecedented succession of extreme environmental events beginning in 2013. Elevated SSTs induced severe island-wide bleaching in 2013, 2014, 2016, and 2017. Additionally, a major ENSO event triggered extreme low tides beginning in 2014 and extending through 2015, causing additional coral mortality from subaerial exposure on shallow reef flat platforms. Here, we present the results of preliminary analyses of environmental and biological data collected during each of these events. Accumulated heat stress in 2013 was the highest since satellite measurements began, but this record was exceeded in 2017. Overall, live coral cover declined by 37% at shallow reef flat sites along the western coast, and by 34% at shallow seaward slope sites around the island. Staghorn Acropora communities lost an estimated 36% live coral cover by 2017. Shallow seaward slope communities along the eastern windward coast were particularly devastated, with an estimated 60% of live coral cover lost between 2013 and 2017. Preliminary evidence suggests that some coral species are at high risk of extirpation from Guam’s waters. In light of predictions of the near-future onset of severe annual bleaching, and the possibility that the events of 2013–2017 may signal the early arrival of these conditions, the persistence of Guam’s current reef assemblages is in question. Here, we present detailed documentation of ongoing changes to community structure and the status of vulnerable reef taxa, as well as a critical assessment of our response protocol, which evolved annually as bleaching events unfolded. Such documentation and analysis are critical to formulating effective management strategies for the conservation of remaining reef diversity and function

Contribution of Rare Copy Number Variants to Bipolar Disorder Risk is Limited to Schizoaffective Cases

Background. Genetic risk for bipolar disorder (BD) is conferred through many common alleles, while a role for rare copy number variants (CNVs) is less clear. BD subtypes schizoaffective disorder bipolar type (SAB), bipolar I disorder (BD I) and bipolar II disorder (BD II) differ according to the prominence and timing of psychosis, mania and depression. The factors contributing to the combination of symptoms within a given patient are poorly understood. Methods. Rare, large CNVs were analyzed in 6353 BD cases (3833 BD I [2676 with psychosis, 850 without psychosis], 1436 BD II, 579 SAB) and 8656 controls. Measures of CNV burden were integrated with polygenic risk scores (PRS) for schizophrenia (SCZ) to evaluate the relative contributions of rare and common variants to psychosis risk. Results. CNV burden did not differ relative to controls in BD when treated as a single diagnostic entity. Burden in SAB was increased relative to controls (p-value = 0.001), BD I (p-value = 0.0003) and BD II (p-value = 0.0007). Burden and SCZ PRS were increased in SAB compared to BD I with psychosis (CNV p-value = 0.0007, PRS p-value = 0.004) and BD I without psychosis (CNV p-value = 0.0004, PRS p-value = 3.9 x 10-5). Within BD I, psychosis was associated with increased SCZ PRS (p-value = 0.005) but not CNV burden. Conclusions. CNV burden in BD is limited to SAB. Rare and common genetic variants may contribute differently to risk for psychosis and perhaps other classes of psychiatric symptoms