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Reproductive Effects of DBCP: It Takes Two to Make a Baby
Published in John R. Goldsmith, Environmental Epidemiology: Epidemiological Investigation of Community Environmental Health Problems, 2019
John R. Goldsmith, Gad Potashnik
One group of scientists has reported a structural abnormality in the Y-chromosome in the spermatozoa of exposed workers.5 We know that the Y-chromosome is the one which determines whether the offspring will be male. These scientists used a fluorescent dye which is known to attach to and stain the Y chromosome. They stained and examined for fluorescence, semen samples from workers exposed to DBCP and from other men, not exposed to known spermatotoxic agents. In both groups, they found approximately the same proportion of stained spermatozoa, so there appeared to be no difference in the proportion of male (stained) and female (unstained) spermatozoa associated with DBCP exposures. But they found something else. The DBCP worker's sperm had a higher proportion of sperm with two staining points, and this difference was statistically significant. They inferred that this reflected what is called “non-dysjunction of the Y-chromosome”. By this was meant that when the sperm cells were being formed in the testes, a larger proportion of them in the DBCP workers failed to separate the two Y-chromosomes, so an increased proportion of the Y-chromosomes were faulty and probably could not fertilize an ovum. Such a method only permits the detection of one possible fault in the production and replication of the Y-chromosomes. Possibly there are other defects in the Y-chromosome or other chromosomes as well.
Radiation and man
Published in R.J. Pentreath, Nuclear Power, Man and the Environment, 2019
Alterations (mutations) to the genes on a chromosome are classified, for convenience, as being either dominant or recessive, depending upon the extent to which the effect is expressed in an offspring which inherits the mutated gene from one parent only. Thus a mutation which is fully dominant will have an effect if inherited from one parent only, whereas a fully recessive mutation has no effect unless the same mutated gene is received from both parents. The only exception is when one mutated gene is associated with the female chromosome. It was stated above that the chromosomes are paired with the exception of the sex chromosomes. Women have 23 matched pairs of chromosomes but in men the 23rd pair do not match. Instead of two large X chromosomes (XX) there is a large X and a small Y chromosome (XY). The Y chromosome carries the gene for maleness and is dominant over the X chromosome. Sperm may have either the X or the Y chromosome, whereas all ova have the X chromosome, and thus all resulting embryos receive at least one X chromosome. The relevance of this is that the X chromosome carries a number of genes which have nothing to do with characteristics of sex, whereas the Y chromosome does not.
Environmental Disease
Published in Gary S. Moore, Kathleen A. Bell, Living with the Earth, 2018
Gary S. Moore, Kathleen A. Bell
Other genetic diseases are inherited as autosomal recessive, which means that a defective gene must occur in both chromosomes at complementary sites in order for the disease to be expressed. It also means that both parents, if healthy, were each carriers of the defective gene, which they passed along to the child. A person with this type of genetic disease is deprived of an essential protein resulting in a potentially severe disease, such as PKU or CF.27 There are also dominant and recessive defective genes on the sex chromosomes as well, producing a variety of sex-linked diseases, including hemophilia-A, color blindness, and forms of muscular dystrophy. Since males have one copy of the Y-chromosome, even recessive sex-linked genetic diseases are expressed in men, as there is no other allele to mask the defect.
Developing gene drive technologies to eradicate invasive rodents from islands
Published in Journal of Responsible Innovation, 2018
Caroline M. Leitschuh, Dona Kanavy, Gregory A. Backus, Rene X. Valdez, Megan Serr, Elizabeth A. Pitts, David Threadgill, John Godwin
Gene editing tools are being used at Texas A&M University to create ‘daughterless’ mice – in other words, mice that are unable to bear female offspring – by inserting the Sry gene sequence into the t-haplotype. The Sry gene is normally located on the Y-chromosome and controls the development of male characteristics. Because the t-haplotype has meiotic drive and is located on an autosome, in order to spread the Sry gene to both XX and XY offspring, the Sry gene has to be copied and inserted into the t-haplotype. This ensures that all offspring receiving the t-allele with the Sry gene, regardless of chromosomal sex, would be phenotypically male (Figure 1; Piaggio et al. 2017). Targeting a construct containing Sry to the t-haplotype should result in nearly all offspring inheriting the Sry gene. Releasing male genetically engineered (GE) mice with the Sry/t-haplotype into a population of wild mice, where they could breed with wild females, could be effective in spreading the Sry/t-haplotype through a population and increasing the relative proportion of male mice in a population.