RESUMO
BACKGROUND: The tea tree (Melaleuca alternifolia) is renowned for its production of tea tree oil, an essential oil primarily composed of terpenes extracted from its shoot. MYB transcription factors, which are one of the largest TF families, play a crucial role in regulating primary and secondary metabolite synthesis. However, knowledge of the MYB gene family in M. alternifolia is limited. METHODS AND RESULTS: Here, we conducted a comprehensive genome-wide analysis of MYB genes in M. alternifolia, referred to as MaMYBs, including phylogenetic relationships, structures, promoter regions, and GO annotations. Our findings classified 219 MaMYBs into four subfamilies: one 5R-MYB, four 3R-MYBs, sixty-one MYB-related, and the remaining 153 are all 2R-MYBs. Seven genes (MYB189, MYB146, MYB44, MYB29, MYB175, MYB162, and MYB160) were linked to terpenoid synthesis based on GO annotation. Phylogenetic analysis with Arabidopsis homologous MYB genes suggested that MYB193 and MYB163 may also be involved in terpenoid synthesis. Additionally, through correlation analysis of gene expression and metabolite content, we identified 42 MYB genes associated with metabolite content. CONCLUSION: The results provide valuable insights into the importance of MYB transcription factors in essential oil production in M. alternifolia. These findings lay the groundwork for a better understanding of the MYB regulatory network and the development of novel strategies to enhance essential oil synthesis in M. alternifolia.
Assuntos
Arabidopsis , Melaleuca , Óleos Voláteis , Genes myb , Melaleuca/genética , Filogenia , Chás Medicinais , Fatores de Transcrição/genética , TerpenosRESUMO
Spinal cord injury (SCI) is a severe neurological disorder and the molecular mechanisms leading to its poor prognosis remain to be elucidated. S100A1, a mediator of Ca2+ handling of sarcoplasmic reticulum and mitochondrial function, operates as an endogenous danger signal (alarmin) associated with inflammatory response and tissue injury. The aim of the present study was to investigate the expression and biological effects of S100A1 in SCI. A rat model of SCI and a PC12 cell model of lipopolysaccharide (LPS)induced inflammation were established to examine S100A1 expression at the mRNA and protein levels. The inflammation level, which was mediated by S100A1, was determined based on inflammatory factor (IL1ß, IL6 and TNFα) and antiinflammatory factor (IL10) expression. The effects of S100A1 on cellular oxidation and antioxidation levels were observed by detecting the levels of reactive oxygen species, superoxide dismutase, catalase activities and nuclear factor erythroid 2related factor 2 expression. The protein levels of Bax, Bcl2 and cleaved caspase3 were used for the evaluation of the effects of S100A1 on apoptosis. Phosphorylated (p)ERK1/2 expression was used to evaluate the effects of S100A1 on ERK signaling. The results revealed that S100A1 expression was significantly upregulated in vivo and in vitro in the PC12 cell model of LPSinflammation. The silencing and overexpression of S100A1 helped alleviate and aggravate LPSinduced inflammation, oxidative stress and apoptosis levels, respectively. S100A1 was found to regulate the ERK signaling pathway positively. An inhibitor of ERK signaling (MK8353) partially abolished the promoting effects of the overexpression of S100A1 on inflammation, oxidative stress damage and apoptosis. In conclusion, S100A1 expression was elevated in model of SCI and in the PC12 cell model of LPSinduced inflammation. Furthermore, the overexpression/silencing S100A1 aggravated/mitigated the inflammation, oxidative stress damage and the apoptosis of LPSstimulated PC12 cells via the ERK signaling pathway. The present study revealed the mechanism of S100A1 in SCI, which provided a new theoretic reference for future research on SCI.