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As global warming threatens their existence, there are widespread concerns regarding the persistence of lime-sand islands and the future of mid-ocean atoll nations. To investigate how climate change has affected lime-sand islands, changes in vegetation and other characteristics of such islands in the South China Sea (SCS) were investigated from 1989 to 2019 using 67 satellite images. First, boundaries of the lime-sand islands and their vegetation were extracted using an active contour extraction procedure called the gradient vector flow snake model. Afterwards, the spatial extents were estimated by enclosing the extracted boundaries, and the digital shoreline analysis system was used to calculate beach widths. Finally, area growth rates and speeds were used to evaluate areal changes in the lime-sand islands and their respective vegetation. Based on the estimated area growth rates, area growth speeds, and beach widths, the lime-sand islands in SCS eroded over the past three decades whereas their vegetation expanded. Further analysis suggested that direct inundation caused by sea-level rise might not be clearly identified from the satellite images. However, other climate change-related factors were most likely responsible for the observed island erosions. These factors included higher wave energy, stronger typhoon intensity and destructiveness, and accelerated coral reef degradation. In addition, the observed expansion of vegetation on the lime-sand islands was likely due to the increase in precipitation in a warming world. The results show that 1) the lime-sand islands will continue to erode whereas vegetation will continue to expand; 2) As vegetation growth is significantly inhibited by salt water when it is adjacent to the ocean, vegetation areas on lime-sand islands may start to continuously decline. Overall, this study is the first to quantitatively examine changes in SCS lime-sand islands due to global warming.

Expression of the hominoid-specific oncoprotein TBC1D3 promotes enhanced cell growth and proliferation by increased activation of signal transduction through several growth factors. Recently we documented the role of CUL7 E3 ligase in growth factors-induced ubiquitination and degradation of TBC1D3. Here we expanded our study to discover additional molecular mechanisms that control TBC1D3 protein turnover. We report that TBC1D3 is palmitoylated on two cysteine residues: 318 and 325. The expression of double palmitoylation mutant TBC1D3:C318/325S resulted in protein mislocalization and enhanced growth factors-induced TBC1D3 degradation. Moreover, ubiquitination of TBC1D3 via CUL7 E3 ligase complex was increased by mutating the palmitoylation sites, suggesting that depalmitoylation of TBC1D3 makes the protein more available for ubiquitination and degradation. The results reported here provide novel insights into the molecular mechanisms that govern TBC1D3 protein degradation. Dysregulation of these mechanisms in vivo could potentially result in aberrant TBC1D3 expression and promote oncogenesis.