The mate competition hypothesis involves the prediction that a human with a larger penis would be able to displace the sperm of another. Studies have found that larger penises do not displace other sperm more effectively than smaller penises, but rather longer penises may ejaculate sperm inside the vagina in places that would be harder for a following penis to displace. The depth of pelvic thrusting was correlated to the displacement of competing sperm. See also
Digit ratio
Human vaginal size
Jonah Falcon
Penis enlargement
Penis envy
Phalloplasty
Sexual selection in humans
The Third Chimpanzee
Why Is Sex Fun? References
Citations
General and cited sources
"Men worry more about penile size than women, says 60-year-old research review" (Press release). Blackwell. 31 May 2007. Retrieved 11 August 2018. Lee, P. A; Mazur, T; Danish, R; Amrhein, J; Blizzard, R. M; Money, J; Migeon, C. J (1980). "Micropenis. I. Criteria, etiologies and classification". The Johns Hopkins Medical Journal. 146 (4): 156–63. PMID 7366061. NAID 10010056499. Lauersen, Niels; Whitney, Steven (1983). Its Your Body: A Womans Guide to Gynecology (3rd ed.). New York: Berkley Publishing. p. 480. ISBN 978-0-425-09917-9. Rushton, J.Philippe; Bogaert, Anthony F (1987). "Race differences in sexual behavior: Testing an evolutionary hypothesis". Journal of Research in Personality. 21 (4): 529–51. doi:10.1016/0092-6566(87)90038-9. Sutherland, Ronald S; Kogan, Barry A; Baskin, Laurence S; Mevorach, Robert A; Conte, Felix; Kaplan, Selna L; Grumbach, Melvin M (1996). "The Effect of Prepubertal Androgen Exposure on Adult Penile Length". The Journal of Urology. 156 (2): 783–7, discussion 787. doi:10.1016/S0022-5347(01)65814-2. PMID 8683783. == External links ==
When recognized by the spliceosome, the sequence between the original and duplicated AGGT will be spliced, resulting in the creation of an intron without alteration of the coding sequence of the gene. Double-stranded break repair via non-homologous end joining was recently identified as a source of intron gain when researchers identified short direct repeats flanking 43% of gained introns in Daphnia. These numbers must be compared to the number of conserved introns flanked by repeats in other organisms, though, for statistical relevance. For group II intron insertion, the retrohoming of a group II intron into a nuclear gene was proposed to cause recent spliceosomal intron gain. Intron transfer has been hypothesized to result in intron gain when a paralog or pseudogene gains an intron and then transfers this intron via recombination to an intron-absent location in its sister paralog. Intronization is the process by which mutations create novel introns from formerly exonic sequence. Thus, unlike other proposed mechanisms of intron gain, this mechanism does not require the insertion or generation of DNA to create a novel intron.The only hypothesized mechanism of recent intron gain lacking any direct evidence is that of group II intron insertion, which when demonstrated in vivo, abolishes gene expression. Group II introns are therefore likely the presumed ancestors of spliceosomal introns, acting as site-specific retroelements, and are no longer responsible for intron gain.