Supplementary Figures S1-S5 and Legends from AMPK–ULK1-Mediated Autophagy Confers Resistance to BET Inhibitor JQ1 in Acute Myeloid Leukemia Stem Cells

Supplementary figure S1. Differential sensitivity of human AML LSCs to JQ1. Supplementary figure S2. Relative levels of the autophagy pathway effectors LC3-II, beclin-1, and pULK1 (S555). Supplementary figure S3. Autophagy induction in KG1 and KG1a cells and effects of autophagy inhibition on JQ1-induced apoptosis in LSCs. Supplementary figure S4. JQ1-induced apoptosis through intrinsic apoptosis pathway in JQ1-sensitive LSCs. Supplementary figure S5. Diagram illustrating the potential effects of the BET inhibitor JQ1 in JQ1-resistant LSCs.</p

Supplemental Table 2 from AMPK–ULK1-Mediated Autophagy Confers Resistance to BET Inhibitor JQ1 in Acute Myeloid Leukemia Stem Cells

Patient characteristics according to JQ1 sensitivity in primary acute myeloid leukemia blasts</p

Supplemental Table 1 from AMPK–ULK1-Mediated Autophagy Confers Resistance to BET Inhibitor JQ1 in Acute Myeloid Leukemia Stem Cells

Effects of JQ1 on phenotypes and apoptosis of primary acute myeloid leukemia stem cells from 13 patietns</p

Additional file 1 of PERK/NRF2 and autophagy form a resistance mechanism against G9a inhibition in leukemia stem cells

Additional file 1: Table S1. Synergistic effects of the G9a and PERK inhibitor on apoptosis of primary acute myeloid LSCs. Figure S1. Effects of treatment with the PERK inhibitor GKS2606414 for 48 h in the presence or absence of 10 μM BIX-01294, on apoptosis. Figure S2. Effect of PERK inhibition on BIX-01294- induced apoptosis in KG1a cells. (A) KG1a cells were treated with 10 μM BIX-01294 in the presence or absence of the PERK inhibitor GSK260641 at 5 μM. After incubation for 48 h, the apoptotic fraction was measured using flow-cytometric analysis. (B) KG1a cells were transfected with PERK siRNA or scrambled siRNA as described in the Materials and Methods and then treated with 10 μM BIX-01294 for 48 h. Figure S3. Effects of treatment for 48 h with the NRF2 inhibitor brusatol in the presence or absence of 10 μM BIX-01294 on apoptosis. Figure S4. Effects of PERK inhibition in the absence or presence of 2 nM bafilomycin A1 on autophagy induction

Table_1_The Origin of the Subtropical Coral Alveopora japonica (Scleractinia: Acroporidae) in High-Latitude Environments.DOCX

Marine ecosystems in temperate regions have been significantly affected by rising seawater temperatures due to climate change. Alveopora japonica, a small zooxanthellate scleractinian coral, occurs in the northwestern Pacific including Taiwan, Japan, and Jeju Island in Korea. The northern populations around Jeju Island have recently undergone rapid growth in numbers, with negative impacts on local biodiversity. However, it is unclear whether these Korean populations occurred historically and where they originate from. In this study, we investigated the phylogenetic relationships of A. japonica along with its endosymbiont Symbiodiniaceae across five geographic regions, including Jeju Island in Korea, Taiwan, and Japan. Nuclear internal transcribed spacer (ITS) sequences revealed unexpected species-level divergence among three distinct phylogenetic clusters (Korea, Taiwan, and Japan) with no sharing of haplotypes among lineages, suggesting these may each represent cryptic species in Alveopora. 23S ribosomal DNA of Symbiodiniaceae showed two well-separated phylogenetic clusters, in which Korean and Japanese symbionts shared the same clade and Taiwanese ones formed a distinct clade. Given the deep phylogenetic divergences among the lineages for both corals and Symbiodiniaceae, the Korean populations appear to have existed for a long evolutionary time period rather than representing a poleward migration from subtropical environments following recent climate change. Our study highlights cryptic species diversity in Alveopora at high-latitude environments.</p