Date: September 2, 2016
Source: CNRS
It was already known that genes
inherited from ancient retroviruses[1] are essential to the placenta in
mammals, a finding to which scientists in theLaboratoire Physiologie et
Pathologie Moléculaires des Rétrovirus Endogènes et Infectieux(CNRS/Université
Paris-Sud) contributed. Today, the same scientists[2] have revealed a new
chapter in this astonishing story: these genes of viral origin may also be
responsible for the more developed muscle mass seen in males! Their findings
are published on 2 September 2016 in PLOS Genetics.
Retroviruses carry proteins on
their surface that are able to mediate fusion of their envelope with the
membrane of a target cell. Once released inside that cell, their genetic
material becomes integrated in the host's chromosomes. In the rare cases where
the infected cell is involved in reproduction, the viral genes may be
transmitted to progeny. Thus nearly 8% of the mammalian genome is made up of
vestiges of retroviruses, or "endogenous" retroviruses. Most of them
are inactive, but some remain capable of producing proteins: this is the case
of syncytins, proteins that are present in all mammals and encoded by genes
inherited from retroviruses "captured" by their ancestors. A little
more than five years ago, and thanks to inactivation of these genes in mice,
the team led by Thierry Heidmann demonstrated that syncytins contribute to
formation of the placenta. Because of their ancestral ability to mediate
cell-cell fusion they give rise to the syncytiotrophoblast[3], a tissue formed
by the fusion of a large number of cells derived from the embryo, at the
fetomaternal interface.
Using the same mice, the team has
revealed a "collateral" and unexpected effect of these proteins: they
endow males with more muscle mass than females! Like the syncytiotrophoblast,
muscle mass develops from fused stem cells. In the genetically-modified male
mice, these fibers were 20% smaller and displayed 20% fewer nuclei than in
standard males; they were then similar to those seen in females, as was their
total muscle mass. It therefore appears that the inactivation of syncytins
leads to a fusion deficit during muscle growth, but only in males. The
scientists observed the same phenomenon in the case of muscle regeneration
following a lesion: the male mice incapable of producing syncytins experienced
less effective regeneration than the other males, but it was comparable to that
seen in females. Furthermore, the regenerating muscle fibers produced syncytin
-- once again, only in males.
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