Fine-suspended sediment and water budgets for a large, seasonally dry tropical catchment: Burdekin River catchment, Queensland, Australia

The Burdekin River catchment (~130,400 km2) is a seasonally dry tropical catchment located in north-east Queensland, Australia. It is the single largest source of suspended sediment to the Great Barrier Reef (GBR). Fine sediments are a threat to ecosystems on the GBR where they contribute to elevated turbidity (reduced light), sedimentation stress, and potential impacts from the associated nutrients. Suspended sediment data collected over a 5 year period were used to construct a catchment-wide sediment source and transport budget. The Bowen River tributary was identified as the major source of end-of-river suspended sediment export, yielding an average of 530 t km−2 yr−1 during the study period. Sediment trapping within a large reservoir (1.86 million ML) and the preferential transport of clays and fine silts downstream of the structure were also examined. The data reveal that the highest clay and fine silt loads—which are of most interest to environmental managers of the GBR—are not always sourced from areas that yield the largest total suspended sediment load (i.e., all size fractions). Our results demonstrate the importance of incorporating particle size into catchment sediment budget studies undertaken to inform management decisions to reduce downstream turbidity and sedimentation. Our data on sediment source, reservoir influence, and subcatchment and catchment yields will improve understandings of sediment dynamics in other tropical catchments, particularly those located in seasonally wet-dry tropical savannah/semiarid climates. The influence of climatic variability (e.g., drought/wetter periods) on annual sediment loads within large seasonally dry tropical catchments is also demonstrated by our data

YY1 haploinsufficiency causes an intellectual disability syndrome featuring transcriptional and chromatin dysfunction

Yin and yang 1 (YY1) is a well-known zinc-finger transcription factor with crucial roles in normal development and malignancy. YY1 acts both as a repressor and as an activator of gene expression. We have identified 23 individuals with de novo mutations or deletions of YY1 and phenotypic features that define a syndrome of cognitive impairment, behavioral alterations, intrauterine growth restriction, feeding problems, and various congenital malformations. Our combined clinical and molecular data define “YY1 syndrome” as a haploinsufficiency syndrome. Through immunoprecipitation of YY1-bound chromatin from affected individuals’ cells with antibodies recognizing both ends of the protein, we show that YY1 deletions and missense mutations lead to a global loss of YY1 binding with a preferential retention at high-occupancy sites. Finally, we uncover a widespread loss of H3K27 acetylation in particular on the YY1-bound enhancers, underscoring a crucial role for YY1 in enhancer regulation. Collectively, these results define a clinical syndrome caused by haploinsufficiency of YY1 through dysregulation of key transcriptional regulators