3 research outputs found
Epigenomic Regulatory Mechanism in Vegetative Phase Transition of Malus hupehensis
In woody plants, phase transitions
substantially affect growth
and development. Although there has been considerable interest in
the regulatory mechanisms underlying phase changes, the associated
epigenetic modifications remain relatively uncharacterized. We examined
the DNA methylation changes and the transcriptional responses in adult
and juvenile Malus hupehensis leaves.
The DNA methylations were 66.61% and 68.3% in the CG context, 49.12%
and 52.44% in the CHG context, and 7.02% and 8.22% in the CHH context
for the adult and juvenile leaves, respectively. The number of differentially
methylated regions in all contexts distributed in the genic regions
varied. Additionally, inhibited DNA methylation in adult leaves activated
the transcription of indole-3-acetic acid related genes in the signaling,
response, and transport pathways. Moreover, the opposite methylation
and expression patterns were observed for the SPL and AP2 family genes between the adult and juvenile
leaves. Both gene families contribute to the M. hupehensis vegetative phase transition. Furthermore, the hyper-/hypomethylation
of the gene body or promoter of transcription factor genes may lead
to up-/downregulated gene expression. The methylation levels of the WRKY (22), NAC (21), ERF (8), WOX (2), KNAT (6), EIN3 (2), SCL (7), ZAT (7), and HSF (4) genes were higher in the adult
leaves than in the juvenile leaves, whereas the opposite pattern was
observed for the TCP (2), MADS-box (11), and DOF (3) genes. An analysis of the correlation
between methylation and transcription indicated the methylation of
the gene body in all contexts and the methylation of the promoter
in the CG and CHG contexts are negatively correlated with gene expression.
However, the methylation of the promoter in the CHH context is positively
correlated with gene expression. These findings reflect the diversity
in the epigenetic regulation of gene expression and may be useful
for elucidating the epigenetic regulatory mechanism underlying the M. hupehensis vegetative phase transition
Transcriptomic and Metabolic Analyses Provide New Insights into the Apple Fruit Quality Decline during Long-Term Cold Storage
Long-term
low-temperature conditioning (LT-LTC) decreases apple
fruit quality, but the underlying physiological and molecular basis
is relatively uncharacterized. We identified 12 clusters of differentially
expressed genes (DEGs) involved in multiple biological processes (i.e.,
sugar, malic acid, fatty acid, lipid, complex phytohormone, and stress-response
pathways). The expression levels of genes in sugar pathways were correlated
with decreasing starch levels during LT-LTC. Specifically, starch-synthesis-related
genes (e.g., BE, SBE, and GBSS genes) exhibited downregulated expression, whereas
sucrose-metabolism-related gene expression levels were up- or downregulated.
The expression levels of genes in the malic acid pathway (ALMT9, AATP1, and AHA2) were upregulated, as well as the content of malic acid in apple
fruit during LT-LTC. A total of 151 metabolites, mainly related to
amino acids and their isoforms, amines, organic acids, fatty acids,
sugars, and polyols, were identified during LT-LTC. Additionally,
35 organic-acid-related metabolites grouped into three clusters, I
(3), II (22), and III (10), increased in abundance during LT-LTC.
Multiple phytohormones regulated the apple fruit chilling injury response.
The ethylene (ET) and abscisic acid (ABA) levels increased at CS2
and CS3, and jasmonate (JA) levels also increased during LT-LTC. Furthermore,
the expression levels of genes involved in ET, ABA, and JA synthesis
and response pathways were upregulated. Finally, some key transcription
factor genes (MYB, bHLH, ERF, NAC, and bZIP genes)
related to the apple fruit cold acclimation response were differentially
expressed. Our results suggest that the multilayered mechanism underlying
apple fruit deterioration during LT-LTC is a complex, transcriptionally
regulated process involving cell structures, sugars, lipids, hormones,
and transcription factors
Transcriptomic and Metabolic Analyses Provide New Insights into the Apple Fruit Quality Decline during Long-Term Cold Storage
Long-term
low-temperature conditioning (LT-LTC) decreases apple
fruit quality, but the underlying physiological and molecular basis
is relatively uncharacterized. We identified 12 clusters of differentially
expressed genes (DEGs) involved in multiple biological processes (i.e.,
sugar, malic acid, fatty acid, lipid, complex phytohormone, and stress-response
pathways). The expression levels of genes in sugar pathways were correlated
with decreasing starch levels during LT-LTC. Specifically, starch-synthesis-related
genes (e.g., BE, SBE, and GBSS genes) exhibited downregulated expression, whereas
sucrose-metabolism-related gene expression levels were up- or downregulated.
The expression levels of genes in the malic acid pathway (ALMT9, AATP1, and AHA2) were upregulated, as well as the content of malic acid in apple
fruit during LT-LTC. A total of 151 metabolites, mainly related to
amino acids and their isoforms, amines, organic acids, fatty acids,
sugars, and polyols, were identified during LT-LTC. Additionally,
35 organic-acid-related metabolites grouped into three clusters, I
(3), II (22), and III (10), increased in abundance during LT-LTC.
Multiple phytohormones regulated the apple fruit chilling injury response.
The ethylene (ET) and abscisic acid (ABA) levels increased at CS2
and CS3, and jasmonate (JA) levels also increased during LT-LTC. Furthermore,
the expression levels of genes involved in ET, ABA, and JA synthesis
and response pathways were upregulated. Finally, some key transcription
factor genes (MYB, bHLH, ERF, NAC, and bZIP genes)
related to the apple fruit cold acclimation response were differentially
expressed. Our results suggest that the multilayered mechanism underlying
apple fruit deterioration during LT-LTC is a complex, transcriptionally
regulated process involving cell structures, sugars, lipids, hormones,
and transcription factors
