Long-read detection of transposable element mobilization in the soma of hypomethylated Arabidopsis thaliana individuals.

#Transposons #SomaticTransposition #Hypomethylation #MET1 #Arabidopsis #LongReadSequencing

https://link.springer.com/article/10.1186/s13059-025-03691-7

Long-read detection of transposable element mobilization in the soma of hypomethylated Arabidopsis thaliana individuals - Genome Biology

Background Because transposable elements (TEs) can cause heritable genetic changes, past work on TE mobility in Arabidopsis thaliana has mostly focused on new TE insertions in the germline of hypomethylated plants. It is, however, well-known that TEs can also be active in the soma, although the high-confidence detection of somatic events has been challenging. Results Here, we leverage the high accuracy of PacBio HiFi long reads to evaluate the somatic mobility of TEs in individuals of an A. thaliana non-reference strain lacking activity of METHYLTRANSFERASE1 (MET1), a major component of the DNA methylation maintenance machinery. Most somatically mobile families coincide with those found in germline studies of hypomethylated genotypes, although the exact TE copies differ. We also discover mobile elements that had been missed by standard TE annotation methods. Somatic TE activity is variable among individual plants, but also within TE families. Finally, our approach points to the possible involvement of alternative transposition as a cause for somatic hypermutability in a region that contains two closely spaced VANDAL21 elements. Conclusions Long-read sequencing reveals widespread TE transposition in the soma of A. thaliana hypomethylated mutants. Assessing somatic instead of germline mobilization is a fast and reliable method to investigate different aspects of TE mobility at the single plant level.

SpringerLink
Team reports on relationship between contents of diosgenin and brassinosteroids in Dioscorea zingiberensis

Diosgenin, a secondary metabolite isolated from the Dioscorea spp. plant family, is an irreplaceable and ideal starting material for the synthesis of steroid hormone drugs. Dioscorea zingiberensis is the world's most desirable and important plant source of steroid hormone drugs.

Phys.org
Identification of methylation-regulated genes modulating microglial phagocytosis in hyperhomocysteinemia-exacerbated Alzheimer’s disease. https://doi.org/10.1186/s13195-023-01311-9 #Alzheimer’s #Hyperhomocysteinemia #Microglia #Phagocytosis #Hypomethylation
Identification of methylation-regulated genes modulating microglial phagocytosis in hyperhomocysteinemia-exacerbated Alzheimer’s disease - Alzheimer's Research & Therapy

Background Hyperhomocysteinemia (HHcy) has been linked to development of Alzheimer’s disease (AD) neuropathologically characterized by the accumulation of amyloid β (Aβ). Microglia (MG) play a crucial role in uptake of Aβ fibrils, and its dysfunction worsens AD. However, the effect of HHcy on MG Aβ phagocytosis remains unstudied. Methods We isolated MG from the cerebrum of HHcy mice with genetic cystathionine-β-synthase deficiency (Cbs−/−) and performed bulk RNA-seq. We performed meta-analysis over transcriptomes of Cbs−/− mouse MG, human and mouse AD MG, MG Aβ phagocytosis model, human AD methylome, and GWAS AD genes. Results HHcy and hypomethylation conditions were identified in Cbs−/− mice. Through Cbs−/− MG transcriptome analysis, 353 MG DEGs were identified. Phagosome formation and integrin signaling pathways were found suppressed in Cbs−/− MG. By analyzing MG transcriptomes from 4 AD patient and 7 mouse AD datasets, 409 human and 777 mouse AD MG DEGs were identified, of which 37 were found common in both species. Through further combinatory analysis with transcriptome from MG Aβ phagocytosis model, we identified 130 functional-validated Aβ phagocytic AD MG DEGs (20 in human AD, 110 in mouse AD), which reflected a compensatory activation of Aβ phagocytosis. Interestingly, we identified 14 human Aβ phagocytic AD MG DEGs which represented impaired MG Aβ phagocytosis in human AD. Finally, through a cascade of meta-analysis of transcriptome of AD MG, functional phagocytosis, HHcy MG, and human AD brain methylome dataset, we identified 5 HHcy-suppressed phagocytic AD MG DEGs (Flt1, Calponin 3, Igf1, Cacna2d4, and Celsr) which were reported to regulate MG/MΦ migration and Aβ phagocytosis. Conclusions We established molecular signatures for a compensatory response of Aβ phagocytosis activation in human and mouse AD MG and impaired Aβ phagocytosis in human AD MG. Our discoveries suggested that hypomethylation may modulate HHcy-suppressed MG Aβ phagocytosis in AD.

BioMed Central