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DNA that’s been preserved from bygone viral infections is essential to embryonic growth, a study implies.(Image credit: fotograzia via Getty Images)ShareShare by:
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A fragment of DNA within the mouse’s genetic structure, inherited from former viral infections, is key for initial progress while in utero, according to novel research.
As shown in the investigation, reported in December in the journal Science Advances, this viral DNA triggers genes that grant cells from mouse embryos in their early stages the capability of transforming into nearly any cell variety in the body. This viral DNA — identified as MERVL — becomes operative itself thanks to a protein referred to as the “Dux transcription factor,” which affixes to the sequence and, in essence, commences the embryo’s growth.
This recent study illuminates not only the functions fulfilled by MERVL and Dux within the womb but also distinguishes between the detrimental impacts they could induce later on in life. It represents an “important piece of work,” in the words of Sherif Khodeer, a postdoctoral research fellow concentrating on stem cell and developmental biology at the university KU Leuven who did not participate in the study.
A powerful gene-editing tool
Researchers operating at the Medical Research Council Laboratory of Medical Sciences in England made use of a gene-modifying mechanism termed CRISPR activation (CRISPRa) with the intention of disentangling the intimate association between Dux and MERVL. Unlike conventional CRISPR, which cleaves DNA for the purpose of altering its code, CRISPRa heightens the action of specified genes whilst keeping the underlying DNA order intact.
The team employed CRISPRa in order to activate either Dux or MERVL inside mouse embryonic stem cells. This equipped the scientists to scrutinize the ways in which each element exerted influence over initial embryonic progression.
As soon as the researchers selectively activated MERVL, the stem cells exhibited “totipotency,” which is the capacity to transform into any cell type — a noteworthy attribute characterizing the earliest embryos. However, the cells were devoid of certain key features, the researchers determined. That implies that, despite MERVL fulfilling a significant role in early mouse embryo development, the presence of Dux is also necessary.
Conversely, activating Dux alone resulted in cells that were substantially more comparable to natural early embryonic cells. Thus, the researchers posit that Dux triggers the genes vital for the embryo’s growth, separate from MERVL.
Due to the tight bond between Dux and MERVL during the starting phases of embryonic development, scientists had earlier entertained the possibility that MERVL may also contribute to Dux’s damaging effects later on in life. However, the novel study suggests that such is not the circumstance.
The researchers evaluated the method by which Dux induces cell detriment by examining its influence on stem cells with and without a gene known as NOXA, which possesses a known involvement in cell death brought on by various stressors. They discovered that Dux activates this NOXA gene, which yields a protein that sets off cell death. Upon removing NOXA, Dux inflicted substantially less harm. That demonstrated that NOXA bears the liability for the toxicity, not MERVL.
A potential therapeutic target
It had already been established that NOXA levels were increased in FSHD, the human muscle-wasting disease. It is conceivable that fabricating a pharmaceutical agent intended to restrain NOXA could avert cell death in the condition, thereby assisting in the enhancement of muscle cell endurance, the study’s creators contemplate.
“Facioscapulohumeral muscular dystrophy is an intricate ailment,” declared senior study author Michelle Percharde, who presides over the chromatin and development group at the Medical Research Council Laboratory of Medical Sciences, in a statement.
“Although every single cell of a patient encompasses the genetic mutations liable for instigating it, only a fraction of cells engage DUX4,” she clarified. “Acquiring an understanding of the stimuli responsible for setting off DUX4 activation exclusively in muscle cells, and the extent to which this compares to activation during initial development, constitute pivotal issues we aspire to probe in subsequent inquiries.”
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It would be “beneficial to juxtapose” the operational characteristics of mouse Dux and human DUX4, Khodeer stated, further noting that successive studies ought to explore the specific manner in which MERVL regulates nearby genes, along with the timing and means by which MERVL deactivates throughout mouse embryo progression.
Significantly, Khodeer underscored the fact that MERVL is absent within the human genome. However, scientists harbor suspicions that particular portions of the human genome might bear equivalence to MERVL. Analogous to mice, these segments of DNA are legacies of earlier viral infections.
Khodeer conveyed that the present findings bring forth several queries. For example, do human embryos in their early stages advance through similar mechanisms observed in mice? And which elements of primeval viral DNA in humans may fulfill roles akin to MERVL at such an early phase of development? “Resolving these inquiries could elucidate disparities in early developmental regulation particular to individual species,” he stated to Live Science via email.
Clarissa BrincatLive Science Contributor
Clarissa Brincat functions as a freelance writer with a focus on matters of health and medical research. Following the attainment of an MSc in chemistry, she ascertained a preference for writing in the realm of science as opposed to conducting it. She garnered expertise in editing scientific documents during a period as a chemistry copyeditor, ultimately transitioning to a medical writer post at a healthcare enterprise. Penning content for doctors and authorities holds value, but Clarissa aspired to engage a broader demographic, which naturally steered her toward freelance health and science authorship. Her body of work has additionally been featured in Medscape, HealthCentral, and Medical News Today.
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