Recently I have been thinking of possible and possibly engineered plagues of males. A disrupted sex ratio can, in principle, drive a species extinct. Consider an abnormal genome which causes a male to produce only male sperm. This could, in principle spread through a population causing a shortage of females and reduced fitness. The key point is that males are healthy (well some are) but that the number of females typically limits total reproduction.
My thoughts started with mosquitoes -- in particular Anopheles G, the malarial mosquito. There are 3 key aspects of my almost limitless ignorance. First can mosquitoes be manipulated genetically (yes they are getting there). Second how is mosquito sex determined ? There appears to be a gene whose dominant allele causes maleness (good)
A. aegypti and other culicine mosquitoes lack heteromorphic sex chromosomes . Instead, sex is controlled by an autosomal locus wherein the male-determining allele, M, is dominant.
Finally, it is key to find a mostquito transposon -- this is a DNA sequence which makes copies of itself. They are useful as a means of getting engineered DNA into chromosomes and act as extremely benign viruses spreading without hurting their hosts. I asked Google and found a paper published last year
A synthetic homing endonuclease-based gene drive system in the human malaria mosquito
Nikolai Windbichler, Miriam Menichelli, Philippos Aris Papathanos, Summer B. Thyme, Hui Li, Umut Y. Ulge, Blake T. Hovde, David Baker, Raymond J. Monnat, Austin Burt & Andrea Crisanti AffiliationsContributionsCorresponding author Nature 473, 212–215 (12 May 2011) doi:10.1038/nature09937 Received 28 September 2010 Accepted 16 February 2011 Published online 20 April 2011
Windbichler et al are interested in using their selfish gene to spread Malaria resistance in a population. I think it could also be used to spread maleness (I don't really know that the M allele has been closed) driving the species extinct. The advantage of this approach is that sex is species specific, so environmental disruption is limited and competing species are not handicapped.
Genetic methods of manipulating or eradicating disease vector populations have long been discussed as an attractive alternative to existing control measures because of their potential advantages in terms of effectiveness and species specificity1, 2, 3. The development of genetically engineered malaria-resistant mosquitoes has shown, as a proof of principle, the possibility of targeting the mosquito’s ability to serve as a disease vector4, 5, 6, 7. The translation of these achievements into control measures requires an effective technology to spread a genetic modification from laboratory mosquitoes to field populations8. We have suggested previously that homing endonuclease genes (HEGs), a class of simple selfish genetic elements, could be exploited for this purpose9. Here we demonstrate that a synthetic genetic element, consisting of mosquito regulatory regions10 and the homing endonuclease gene I-SceI11, 12, 13, can substantially increase its transmission to the progeny in transgenic mosquitoes of the human malaria vector Anopheles gambiae. We show that the I-SceI element is able to invade receptive mosquito cage populations rapidly, validating mathematical models for the transmission dynamics of HEGs. Molecular analyses confirm that expression of I-SceI in the male germline induces high rates of site-specific chromosomal cleavage and gene conversion, which results in the gain of the I-SceI gene, and underlies the observed genetic drive. These findings demonstrate a new mechanism by which genetic control measures can be implemented. Our results also show in principle how sequence-specific genetic drive elements like HEGs could be used to take the step from the genetic engineering of individuals to the genetic engineering of populations.
Less practically, male plagues have surely occurred. The only way to escape is to speciate -- females who don't mate with the infectiously male males do fine. This means that male plagues might tend to eliminate most of a species leaving a few small isolated populations. This might have promoted speciation for all I know.
update: My mistake. I didn't understand "culicine" anopheles g (the Malaria mosquito) is not culicine and has X and Y chromasomes as we do posted by Robert
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