Adipose tissue is the largest energy reservoir and secretory organ in the animal body, and is essential for maintaining normal physiological functions and metabolic balance. MicroRNAs regulate the process of adipogenic differentiation through post-transcriptional regulatory mechanisms. In the present study, miR-424 was upregulated during bovine adipocyte differentiation both in vivo and in vitro. The overexpression and interference of miR-424 exhibited the positive regulatory role in the differentiation of bovine adipocytes. Furthermore, miR-424 directly binds to the three prime untranslated region (3' UTR) of serine/threonine kinase 11 (STK11, also called LKB1), a master upstream gene in the AMP-activated protein kinase (AMPK) cascade, and up-regulates its expression. Functional studies showed that the knockdown of STK11 attenuated the pro-adipogenic effect of miR-424. Post-transcriptional regulation of STK11 by miR-424 was mediated potentially in an RNA binding protein (RBP) binding site-dependent manner. In conclusion, our study shows that miR-424 promotes bovine adipogenesis through an unconventional post-transcriptional regulation of STK11, which may serve as a potential target for the regulation of bovine adipogenesis and the improvement of livestock breeding efficiency. Copyright © 2020 Wang, Zhang, Zhang, Cheng, Khan, Junjvlieke, Li and Zan.The dominant white phenotype in pigs is thought to be mainly due to a structural mutation in the KIT gene, a splice mutation (G > A) at the first base in intron 17 which leads to the deletion of exon 17 in the mature KIT mRNA. However, this hypothesis has not yet been validated by functional studies. Here, we created two mouse models, KIT D17/+ to mimic the splice mutation, and KIT Dup/+ to partially mimic the duplication mutation of KIT gene in dominant white pigs using CRISPR/Cas9 technology. We found that the splice mutation homozygote is lethal and the heterozygous mice have a piebald coat. Slightly increased expression of KIT in KIT Dup/+ mice did not confer the patched phenotype and had no obvious impact on coat color. Interestingly, the combination of these two mutations reduced the phosphorylation of PI3K and MAPK pathway associated proteins, which may be related to the impaired migration of melanoblasts observed during embryonic development that eventually leads to the dominant white phenotype. Copyright © 2020 Sun, Liang, Qin, Qin, Shi, Cong, Mo, Liu, Chen and He.Some differentially expressed genes (DEGs) that encode key enzymes involved in steroidogenic biosynthesis (CYP19A1) and key molecules related to gonadal functions (DMRT1, SOX9, AMH, FOXL2, WNT4, RSPO2, and GDF9) have been identified in adult gonadal RNA-seq studies of Reeves' pond turtle (Mauremys reevesii) with temperature-dependent sex determination (TSD). learn more Gonadal functional maintenance and gametogenesis comprises a highly regulated and coordinated biological process, and increasing evidence indicates that microRNAs (miRNAs) may be involved in this dynamic program. However, it is not clear how the regulatory network comprising miRNAs changes the expression levels of these genes. In this study, miRNA sequencing of adult testis and ovary tissues from M. reevesii detected 25 known and 379 novel miRNAs, where 60 miRNAs were differentially expressed in the testis and ovary. A total of 1,477 target genes based on the differentially expressed miRNAs were predicted, where 221 target genes also exhibited differential expression. To verify the accuracy of the sequencing data, 10 differentially expressed miRNAs were validated by quantitative reverse transcription real-time PCR, and were found to be consistent with the transcriptome sequencing results. Moreover, several miRNA/target gene pairs, i.e., mre-let-7a-5p/mre-let-7e-5p and CYP19A1, mre-miR-200a-3p and DMRT1, mre-miR-101-3p and SOX9, and mre-miR-138-5p and AMH were identified. To explore the regulatory role of miRNAs, we conducted target gene enrichment analysis of the miRNAs and 221 target genes in the regulatory network. The signaling pathways related to gonadal functional maintenance and gametogenesis based on the DEGs and target genes were then compared. Our findings provide crucial information to facilitate further research into the regulatory mechanisms involving miRNAs in turtle species with TSD. Copyright © 2020 Xiong, Yang, Zheng, Wang, Gu, Tong, Liu, Shah and Nie.Dystrophinopathies are inherited diseases caused by mutations in the dystrophin (DMD) gene for which testing is mandatory for genetic diagnosis, reproductive choices and eligibility for personalized trials. We genotyped the DMD gene in our Italian cohort of 1902 patients (BMD n = 740, 39%; DMD n =1162, 61%) within a nationwide study involving 11 diagnostic centers in a 10-year window (2008-2017). In DMD patients, we found deletions in 57%, duplications in 11% and small mutations in 32%. In BMD, we found deletions in 78%, duplications in 9% and small mutations in 13%. In BMD, there are a higher number of deletions, and small mutations are more frequent than duplications. Among small mutations that are generally frequent in both phenotypes, 44% of DMD and 36% of BMD are nonsense, thus, eligible for stop codon read-through therapy; 63% of all out-of-frame deletions are eligible for single exon skipping. Patients were also assigned to Italian regions and showed interesting regional differences in mutation distribution. The full genetic characterization in this large, nationwide cohort has allowed us to draw several correlations between DMD/BMD genotype landscapes and mutation frequency, mutation types, mutation locations along the gene, exon/intron architecture, and relevant protein domain, with effects on population genetic characteristics and new personalized therapies. Copyright © 2020 Neri, Rossi, Trabanelli, Mauro, Selvatici, Falzarano, Spedicato, Margutti, Rimessi, Fortunato, Fabris, Gualandi, Comi, Tedeschi, Seia, Fiorillo, Traverso, Bruno, Giardina, Piemontese, Merla, Cau, Marica, Scuderi, Borgione, Tessa, Astrea, Santorelli, Merlini, Mora, Bernasconi, Gibertini, Sansone, Mongini, Berardinelli, Pini, Liguori, Filosto, Messina, Vita, Toscano, Vita, Pane, Servidei, Pegoraro, Bello, Travaglini, Bertini, D'Amico, Ergoli, Politano, Torella, Nigro, Mercuri and Ferlini.