Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • Our results indicate a deregulation of DNA methylation machi

    2020-02-13

    Our results indicate a deregulation of DNA methylation machinery during seed development in apomixis. Since DRM2 is targeted loci through an RNA-directed DNA methylation (RdDM) pathway involving 24-nt siRNAs (Stroud et al., 2014, Law and Jacobsen, 2010) and differentially expressed between apomict and sexual Boechera spp., the genes controlling by this mechanism in natural apomicts may also be important to understand endosperm development in apomixis. This could suggest that such deregulation required for apomixis, but further data is required to establish this. Also, this deregulation specific to apomicts may also trigger epigenetic modifiers during embryo development since apomictic plants do not need paternal genome contributions to produce seeds in Ketorolac tromethamine salt to sexual plants. Therefore, our results showed that epigenetic modifiers regarding to endosperm development in natural apomicts should be investigated further to facilitate transfer of apomixis to crops.
    Acknowledgments We would like to thank to Prof. Dr. M. Eric Schranz (Wageningen University, the Netherlands) for providing the seeds. We also thank to Prof. Dr. Timothy F. Sharbel (Leibniz Institute of Plant Genetics and Crop Plant Research, Germany) for providing partial transcript sequences of DNMT genes.
    Introduction Ultraviolet (UV) radiation is a major risk factor for the induction of skin aging [1]. Prolonged UV exposure accelerates the process of aging by degrading the structural integrity of the dermal extracellular matrix (ECM), resulting in the wrinkled appearance of the skin. The disintegration of each dermal ECM protein is implemented by a large number of proteinases known as matrix metalloproteinases (MMPs). In photoaged skin, an overproduction of MMPs such as MMP1 (interstitial collagenase), MMP3 (stormelysin-1), and MMP9 (gelatinase) and an insufficient amount of collagen synthesis were observed [[2], [3], [4]]. However, these MMP activities were antagonized and inhibited by endogenous matrix metalloproteinase inhibitors, called tissue inhibitor of metalloproteinases (TIMPs) in the dermal layer of the skin [4]. Four members of the TIMP family, designated as TIMP1, TIMP2, TIMP3, and TIMP4, have been identified to regulate metalloproteinase activity [[5], [6], [7]]. While the TIMPs exhibit higher specificity for particular target MMPs, they are capable of interacting with all MMPs [4]. Their functional redundancy has been reported to exist due to their similar expression patterns and shared substrate sites. For instance, TIMP2 interacts with most MMPs, but particularly with MMP2 and MMP9 in the skin [8,9]. In association with UVA irradiation, TIMP2 activity has been shown to decrease in human dermal fibroblasts [10]. Although the epigenetic mechanism accounting for the reduced TIMP2 activity has still yet to be elucidated, a study that performed a transcriptional and genomic analysis of TIMP3 revealed a fully methylated CpG island in cancer cells along with increased DNA methyltransferase 1 (DNMT1) and DNMT3B levels [11]. These results highlight the crucial role of DNA methyltransferases (DNMTs) in executing DNA methylation, and thus, decreasing the expression of TIMPs. DNA methylation involves the addition of a methyl group to the C5 side chain of a cytosine that precede a guanine in the DNA sequence, also known as a “CpG” dinucleotide by DNMTs [12]. According to the long-established but oversimplified model, DNMT1 has been classified as a “maintenance” DNMT because of its role in preserving original methylation patterns, and DNMT3A and DNMT3B, “de novo” methyltransferases, for creating new methylation patterns [12,13]. Another component of the DNA methylation machinery is methyl-cytosine binding domain proteins (MBDs). MBDs acts as an aid to DNMTs by coordinating the recruitment of histone deacetylases (HDACs) to the specific site of methylated DNA, resulting in chromatin condensation and transcriptional silencing [14,15].