The MYB (v-myb avian myeloblastosis viral oncogene homolog) transcription factor family plays an important role in plant growth, development, and response to biotic and abiotic stresses. However, the gene functions of MYB transcription factors in sweet potato (Ipomoea batatas (L.) Lam) have not been elucidated. In this study, an MYB transcription factor gene, IbMYB308, was identified and isolated from sweet potato. Multiple sequence alignment showed that IbMYB308 is a typical R2R3-MYB transcription factor. Further, quantitative real-time PCR (qRT-PCR) analysis revealed that IbMYB308 was expressed in root, stem, and, especially, leaf tissues. Moreover, it showed that IbMYB308 had a tissue-specific profile. The experiment also showed that the expression of IbMYB308 was induced by different abiotic stresses (20% PEG-6000, 200 mM NaCl, and 20% H2O2). After a 200 mM NaCl treatment, the expression of several stress-related genes (SOD, POD, APX, and P5CS) was upregulation in transgenic plants, and the CAT activity, POD activity, proline content, and protein content in transgenic tobacco had increased, while MDA content had decreased. In conclusion, this study demonstrated that IbMYB308 could improve salt stress tolerance in transgenic tobacco. These findings lay a foundation for future studies on the R2R3-MYB gene family of sweet potato and suggest that IbMYB308 could potentially be used as an important positive factor in transgenic plant breeding to improve salt stress tolerance in sweet potato plants.

Relatively little is known regarding mitochondrial metabolism in neuronal differentiation of embryonic stem (ES) cells. By using a small molecule, present research has investigated the pattern of cellular energy metabolism in neural progenitor cells derived from mouse ES cells. Flavonoid compound 4a faithfully facilitated ES cells to differentiate into neurons morphologically and functionally. The expression and localization of peroxisome proliferator-activated receptors (PPARs) were examined in neural progenitor cells. PPAR-β expression showed robust upregulation compared to solvent control. Treatment with PPAR-β agonist L165041 alone or together with compound 4a significantly promoted neuronal differentiation, while antagonist GSK0660 blocked the neurogenesis-promoting effect of compound 4a. Consistently, knockdown of PPAR-β in ES cells abolished compound 4a-induced neuronal differentiation. Interestingly, we found that mitochondrial fusion protein Mfn2 was also abolished by sh-PPAR-β, resulting in abnormal mitochondrial Ca2+ ([Ca2+]M) transients as well as impaired mitochondrial bioenergetics. In conclusion, we demonstrated that by modulating mitochondrial energy metabolism through Mfn2 and mitochondrial Ca2+, PPAR-β took an important role in neuronal differentiation induced by flavonoid compound 4a.

In the present study, we explored the possible links between Junctophilin 2 (Jp2) and the mitochondrium-sarcoplasmic reticulum (SR) interaction in embryonic stem cell-derived cardiomyocytes (ESC-CMs), as well as the role of Jp2 in cardiogenesis of ES cells. We found that Ca(2+) transient was abnormal and mitochondria were de-energized within siJp2 ESC-CMs. The essential juxtaposition structure of mitochondrium with SR was destroyed accompanied by selectively downregulation of Pgc-1α, Nrf-1, and Mfn-2. Impaired co-localization of the JP2 and sarcomeres (α-Actinin or Troponin-T) appeared in embryoid bodies (EBs) after Jp2 knockdown. Calsequestrin2 and ryanodine receptor 2 within SR were expressed as early as the initiation of differentiation, while triadin and caveolin3 within t-tubules (TTs) did not appear until the terminal, indicating that JP2 probably did not contribute to anchoring the SR to TTs at the early cardiogenesis stage as usual. In addition, Jp2 knockdown selectively decreased gene transcription toward cardiogenesis (Brachyury, Isl1, and Nkx2.5), subsequently weaken EB beating activity by 60%. Taken together, reducing JP2 expression in ESC-CMs resulted in impaired mitochondrial status due to either abnormal cellular Ca(2+) homeostasis or disturbing of juxtaposition. A sensitive time window of JP2 necessary in cardiac differentiation was found at early stage via an extra non-TTs/SR anchor-dependent role.

The sweet potato weevil (Cylas formicarius) is an important pest in the growing and storage of sweet potatoes. It is a common pest in the sweet potato production areas of southern China, causing serious harm to the development of the sweet potato industry. For the existing cultivars in China and abroad, there is no sweet potato variety with complete resistance to the sweet potato weevil. Thus, understanding the regulation mechanisms of sweet potato weevil resistance is the prerequisite for cultivating sweet potato varieties that are resistant to the sweet potato weevil. However, very little progress has been made in this field. In this study, we inoculated adult sweet potato weevils into sweet potato tubers. The infected sweet potato tubers were collected at 0, 24, 48, and 72 h. Then, a miRNA library was constructed for Eshu 6 and Guang 87 sweet potato tubers infected for different lengths of time. A total of 407 known miRNAs and 298 novel miRNAs were identified. A total of 174 differentially expressed miRNAs were screened out from the known miRNAs, and 247 differentially expressed miRNAs were screened out from the new miRNAs. Moreover, the targets of the differentially expressed miRNAs were predicted and their network was further investigated through GO analysis and KEGG analysis using our previous transcriptome data. More importantly, we screened 15 miRNAs and their target genes for qRT-PCR verification to confirm the reliability of the high-throughput sequencing data, which indicated that these miRNAs were detected and most of the expression results were consistent with the sequencing results. These results provide theoretical and data-based resources for the identification of miRNAs in response to sweet potato weevil infection and an analysis of the molecular regulatory mechanisms involved in insect resistance.