Chittka, A. | Search bioRxiv

bioRxiv2022

Co-option of endogenous retroviruses through genetic escape from TRIM28 repression

Endogenous retroviruses (ERVs) have rewired host gene networks through co-option of their enhancers. To explore which ERVs get co-opted and why, we tracked the epigenetic fate of murine IAPEz elements using an in vitro model of embryonic stem cell (ESC) to neural progenitor cell (NPC) differentiation. TRIM28-repression depended on a 190bp sequence, previously shown to confer IAPEzs with retrotransposition activity. A subset of IAPEzs ([~]15%) exhibit genetic divergence from this sequence, which we term escapees. While repressed IAPEzs succumb to a previously undocumented epigenetic handover from H3K9me3 in ESCs to H3K27me3 in NPCs, escapee IAPEzs evade repression, resulting in their transcriptional derepression in NPCs. Escapee IAPEzs enhance expression of nearby neural genes and contribute to gene expression differences between mouse strains, which we discern by employing IAPEz insertion polymorphisms. In sum, co-opted ERVs stem from genetic escapees that have lost vital sequences required for both TRIM28 restriction and autonomous retrotransposition. HIGHLIGHTSO_LITracking the epigenetic fate of ERVs through neural differentiation reveals which ERVs are subject to co-option and why. C_LIO_LIMost ERVs succumb to H3K9me3 deposition in ESCs with H3K27me3 memory in NPCs. C_LIO_LIERVs that act as enhancers to nearby neural genes have undergone genetic escape from TRIM28 repression. C_LIO_LIEpigenetic evasion is an evolutionary trade-off that comes with loss of sequences necessary for retrotransposition. C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=130 SRC="FIGDIR/small/497016v1_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@175b6c0org.highwire.dtl.DTLVardef@1313692org.highwire.dtl.DTLVardef@1f5e33forg.highwire.dtl.DTLVardef@1a5ad3_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstract.C_FLOATNO C_FIG

molecular biology↗

bioRxiv2018

Temporal correlation of elevated PRMT1 gene expression with mushroom body neurogenesis during bumblebee brain development

Proper neural development in insects depends on the controlled proliferation and differentiation of neural precursors. In holometabolous insects, these processes must be coordinated during larval and pupal development. Recently, protein arginine methylation has come into focus as an important mechanism of controlling neural stem cell proliferation and differentiation in mammals. Whether a similar mechanism is at work in insects is unknown. We investigated this possibility by determining the expression pattern of three protein arginine methyltransferase mRNAs (PRMT1, 4 and 5) in the developing brain of bumblebees by in situ hybridisation. We detected expression in neural precursors and neurons in functionally important brain areas throughout development. We found markedly higher expression of PRMT1, but not PRMT4 and PRMT5, in regions of mushroom bodies containing dividing cells during pupal stages at the time of active neurogenesis within this brain area. At later stages of development, PRMT1 expression levels were found to be uniform and did not correlate with actively dividing cells. Our study suggests a role for PRMT1 in regulating neural precursor divisions in the mushroom bodies of bumblebees during the period of neurogenesis.

developmental biology↗