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Viruses play critical role in evolution and survival of the species

Viruses are not always bad. New research shows viruses also play a key evolutionary role in mammals' ability to reproduce and survive.

Scientists obtained their data supporting this by studying laboratory mice and human germline cells. 

They reveal two distinct and fundamental processes underlying germline transcriptomes. They also show that species-specific transcriptomes are fine-tuned by  endogenous retroviruses in the mammalian germline

Germline transcriptomes include all the messenger RNA in germline cells, which contain either the male or female half of chromosomes passed on as inherited genetic material to offspring when species mate. This means that germline transcriptomes define the unique character of sperm and egg to prepare for the next generation of life.

One study explores super-enhancers, which are robust and evolutionally conserved gene regulatory elements in the genome. They fuel a tightly regulated burst of essential germline genes as sperm start to form.

The second study  involves endogenous retroviruses that act as another type of enhancer—gene regulatory elements in the genome—to drive expression of newly evolved genes. This helps fine tune species-specific transcriptomes in mammals like humans, mice, and so on.

Together the studies have significant potential ramifications for clinical practice. Dysregulation of gene expression in the formation of male sperm is closely associated with male infertility and birth defects.

Viruses, especially endogenous retroviruses (ERVs) that are an inherent part of mammalian biology, can dramatically influence gene expression, investigators report. ERVs are molecular remnants of retroviruses that infect the body and over time incorporate into the genome.

What we learn from this study is that, in general, viruses have major roles in driving evolution. In the long-term, viruses have positive impacts to our genome and shape evolution.

Those tests revealed that the the genome-wide reorganization of super-enhancers drives bursts of germline gene expression after germ cells enter meiosis, a specialized form of cell division that produces the haploid genome of germ cells.

The study further demonstrates the molecular process through whichsuper-enhancer switching takes place in germ cells. Super-enhancers are regulated by two molecules that act as gene-burst control switches—the transcription factor A-MYB and SCML2, a critical silencing protein in sperm formation.

Endogenous retroviruses are a group of transposable elements (TEs), mobile genetic elements that account for approximately 40-50 percent of a given mammalian genome. Also referred to as "jumping genes," TEs have long been considered genetic threats because transposition can be harmful if, for example, the process disrupts protein-coding genes.

Building on findings from the 1950s that TEs can function as genetic regulatory elements, Namekawa and his collaborators (Sakashita et al.) produced data showing that ERV-driven mechanisms help fine tune species-specific transcriptomes.


Super-enhancer switching drives a burst in gene expression at the mitosis-to-meiosis transition, Nature Structural & Molecular BiologyDOI: 10.1038/s41594-020-0488-3 ,

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