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Fullenkamp, C.

Publications and source records attributed to Fullenkamp, C..

2 recordsLinked to original sources

Valuation of carbon services produced by wild animals finances conservation

Filling the global biodiversity financing gap will require significant investments from financial markets, which demand credible valuations of ecosystem services and natural capital. However, current valuation approaches discourage investment in conservation because their results cannot be verified using market-determined prices. Here, we bridge the gap between finance and conservation by valuing only wild animals carbon services for which market prices exist. By projecting the future path of carbon service production using a spatially-explicit demographic model, we place a credible value on the carbon-capture services produced by African forest elephants. If elephants were protected, their services would be worth $35.9 billion (24.3-41.2) and store 377 MtC (318-388) across tropical Africa. Our methodology can also place lower bounds on the social cost of nature degradation. Poaching would result in $10-14 billion of lost carbon services. Our methodology enables the integration of animal services into global financial markets with major implications for conservation, local socio-economies, and conservation.

ecology↗

TAZ-CAMTA1 and YAP-TFE3 modulate the basal TAZ/YAP transcriptional program by recruiting the ATAC histone acetyltransferase complex

Epithelioid hemangioendothelioma (EHE) is a vascular sarcoma that metastasizes early and lacks an effective medical therapy. The TAZ-CAMTA1 and YAP-TFE3 fusion proteins are chimeric transcription factors and initiating oncogenic drivers of EHE. A combined proteomic/genetic screen identified YEATS2 and ZZZ3, components of the Ada2a-containing histone acetyltransferase (ATAC) complex, as key interactors of both TAZ-CAMTA1 and YAP-TFE3 despite the dissimilarity of the C terminal fusion partners CAMTA1 and TFE3. An integrative next generation sequencing approach showed the fusion proteins drive expression of a unique transcriptome distinct from TAZ and YAP by simultaneously hyperactivating a TEAD-based transcriptional program and modulating the chromatin environment via interaction with the ATAC complex. Interaction of the ATAC complex with both TAZ-CAMTA1 and YAP-TFE3 indicates the histone acetyltransferase complex is an oncogenic driver in EHE and potentially other sarcomas. Furthermore, the ATAC complex is an enzymatic transcriptional cofactor required for both fusion proteins in EHE, representing a unifying therapeutic target for this sarcoma. Gene fusions are the most common genetic alterations activating TAZ and YAP in cancer, and this study serves as a template for identifying epigenetic modifiers recruited by the C terminal fusion partners of other TAZ/YAP gene fusions occurring in gliomas, carcinomas, and other sarcomas. SummaryTAZ-CAMTA1 and YAP-TFE3 alter the TAZ/YAP transcriptional program by recruiting the ATAC complex and modifying the chromatin landscape.

cancer biology↗