The lack of iron in pregnant mice can cause a small part of the embryos with XY chromosomes, which usually determine the male sex, develop ovaries, which reveals a link between the metabolism of iron and the determination of sex in those mammals.
The research published by Nature already charge of the University of Osaka (Japan), carried out with cultivated cells and mice, indicates that the lack of maternal iron at the cellular level of the uterus affects an enzyme that depends on that mineral and that is the one that activates the gene that determines the male sex.
In mammals, which develop in a controlled uterine environment, the determination of sex is controlled by genetics, that is, if an individual has XX or XY chromosomes.
However, most species are subject to the environmental determination of the sixth, when developing from ovules exposed to variable factors such as temperature, pH or hormones, recalls an article of explanation of the study prepared by the University of Duke (EU).
The team wondered if, in mammals, the maternal environmental factors derived from differences in nutrition, metabolism or regulation of metal levels could be potential sources of variability that could affect embryonic development.
The determination of sex in mammals occurs in the early stages of pregnancy and a key gene of the male is the Sry, which controls the development of the testicles and is found in the Y chromosome.
The researchers, headed by Makoto Tachibana, focused on exploring the possible relationship between iron metabolism and the determination of sex in mammals using mice.
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The lack of iron in pregnancy causes mice that should be male can be female
The result was that factors of the cellular environment regulate the expression of the SRY gene, to influence the result of the determination of the male sex, Nature summary.
When the authors reduced iron levels in cultivated cells at approximately 40% of normal levels, Sry’s expression was largely suppressed, and Xy gonads began to show genetic markers associated with the development of ovaries.
Then, the group proved the effects of short -term iron lack in pregnant mouses, which he administered, for about five days around the time of the determination of embryonic sex, a drug that eliminates that mineral.
The result was that of the 72 young born with XY chromosomes, four developed two ovaries and one ovary and a testicle, the investigation indicates.
To study the effect of long -term iron deficiency, the pregnant females were subjected to a low diet in that substance, which began four weeks before pregnancy and continued for another six, which did not show any effect, until they changed strategy.
There is an enzyme called KDM3A, which is essential to regulate the expression of the SRY gene, which depends on iron for its activity. The team introduced a mutation into the rodents that loses its function to the gene that encodes the aforementioned enzyme.
The result was the investment of male to female sex in two of the 43 XY offspring. In none of the experiments anomalies were observed in the children of mothers with normal iron levels
With EFE information
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