Flowering is a necessary condition and basis for yield in the life cycle of woody fruit trees.  Although there has been considerable interest in the regulatory mechanisms underlying floral induction and flowering, the associated epigenetic modifications remain poorly characterized.  We identified genome-wide DNA methylation changes and the transcriptional responses in axillary buds of ‘Qinguan’ (QA) and ‘Fuji’ (FA) varieties with contrasting flowering behaviors.  The DNA methylation levels were 19.35, 62.96 and 17.68% in FA, and 19.64, 62.49 and 17.86% in QA in the CG, CHG and CHH contexts, respectively.  The number of hypermethylated and hypomethylated differentially methylated regions (DMRs) in different regions contributed to significantly up- and downregulated gene expression.  DNA methylation can positively or negatively regulate gene expression depending on the CG, CHG and CHH contexts and their locations in different regions.  Additionally, the huge differences in transcription of MIKC^c-type MADS-box genes, and multiple flowering genes in multiple flowering pathways (i.e., light, aging, GA and sugar) by changing DNA methylation, contributed to contrasting flowering behaviors in both QA and FA.  Specifically, the floral meristem identity genes (i.e., FT, LEAFY, AP1 and SOC1) exhibited significantly higher expression in QA than FA, but the floral repressors (i.e., SVP, AGL15, and AGL18) showed the opposite trend.  Significant differences in multiple hormone levels were due to differentially expressed genes (DEGs) and their DMRs in hormone synthesis pathways, leading to both contrasting axillary bud outgrowth and flowering behaviors.  These findings reflect the diversity in the epigenetic regulation of gene expression and may be helpful for elucidating the epigenetic regulatory mechanism underlying the axillary bud flowering in apple.

Recently, increasing natural infection cases and experimental animal challenge studies demonstrated domestic cats are susceptible to multiple subtypes influenza A virus (IAV) infections.  Notably, some subtype IAV strains could circulate in domestic cats after cross-species transmission and even infected humans, posing a threat to public health.  Host factors related to viral polymerase activity could determine host range of IAV and acidic nuclear phosphoprotein 32 (ANP32) is the most important one among them.  However, role of cat-derived ANP32 on viral polymerase activity and host range of IAV is still unknown.  In the present study, a total of 10 feline ANP32 (feANP32) splice variants (including 5 feANP32A, 3 feANP32B, and 2 feANP32E) were obtained from domestic cats by RT-PCR.  Sequence alignment results demonstrated amino acid deletions and/or insertions occurred among feANP32 variants, but all feANP32 proteins were primarily localized to cell nucleus.  Minigenome replication systems for several representative IAV strains were established and the support ability of feANP32 on IAV polymerase activity was estimated.  The results indicated that most feANP32A and feANP32B splice variants were able to support all the tested IAV strains, though the support activity of a single feANP32 protein on polymerase activity varied among different IAV strains.  In addition, the role of feANP32 in supporting H3N2 canine influenza virus was determined by investigating viral replication in vitro.  Collectively, our study systematically investigated the support activity of feANP32 on IAV, providing a clue for further exploring the mechanism of susceptibility of cats to IAV.