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The Reproductive Systems of Davidson’s Plum (Davidsonia jerseyana, Davidsonia pruriens and Davidsonia johnsonii) and the Potential for Domestication
Published in Yasmina Sultanbawa, Fazal Sultanbawa, Australian Native Plants, 2017
Frances Eliott, Mervyn Shepherd, Maurizio Rossetto, Robert Henry
Another reason to suspect long-term selfing in D. jerseyana is that inbreeding depression was not apparent in offspring included in fitness trials (see the following) and inbreeding depression is more common in predominantly selfing populations of naturally outcrossing species (Stebbins, 1950). Inbreeding depression results in a reduction in offspring fitness and is caused by increased homozygosity in individuals which can effectively ‘fix’ recessive deleterious mutations in populations or an increase in homozygosity at loci with heterozygote advantage (‘overdominance’) (Charlesworth and Willis, 2009). With prolonged selfing, these deleterious alleles can be purged from a population through selection (Charlesworth and Charlesworth, 1987; Lande and Schemske, 1985), whereby individuals with the lethal allele may not reach reproductive age and as a consequence, the allele is not passed on and is eventually purged from the population. Thus, over a period of time and if the population does not vanish as a consequence of inbreeding, the effects of inbreeding depression are greatly reduced or even eliminated.
Genetic research in Edinburgh, 1964–1979
Published in Kiheung Kim, The Social Construction of Disease, 2006
The simplest case of such interaction would of course occur if the host gene Sinc was actually responsible for providing the genetic template for the coat protein, and the protein coat was itself the hypothetical multimeric structure. Differences in incubation period between s7s7 and p7p7 homozygotes might then be explained if the protein coat coded for by one allele could be produced or assembled into a homomeric protein coat more quickly or readily than the protein coded for by the other. More importantly, the phenomenon of overdominance might be explained if, for some reason, it proved particularly difficult to combine the two different types of coat protein, one coded by s7 and the other by p7, into a heteromeric coat structure (Dickinson 1975: 390; Dickinson and Fraser 1975: 11; Dickinson and Outram 1979: 18). They speculated that agent replication must be very limited, otherwise the small proportion of ‘quick’ homomers would be sufficient to give heterozygote incubation periods at least intermediate between the parental types, or even as short as in the quicker homozygote (Dickinson and Outram 1979: 18). However, the experimental data indicated no such case of shorter incubation time than the parental types.
Psychometric and Faciometric Support for Observable Facial Feminization in Gay Men
Published in Journal of Homosexuality, 2019
Julia M. Robertson, Barbara E Kingsley, Gina C. Ford
A number of these theories have, at their core, the suggestion that phenotypic feminization may be involved. Two such theories involve “balancing selection,” these being heterozygote advantage (sometimes known as “balanced polymorphism” or “overdominance”) and sexually antagonistic selection. In terms of heterozygote advantage, the suggestion is that men heterozygous for homosexual genes may carry a fitness advantage over those homozygous for heterosexual genes. There are a number of possible explanations for this, e.g., through superior sperm competition (MacIntyre & Estep, 1993), enhanced sex drive (McKnight, 1997), or suppressed androgenization with resultantly more feminine personality traits (Miller, 2000; Zeitsch et al., 2008), the latter being a view consistent with female preference for feminized facial features in men (Cunningham, Barbee, & Pike, 1990; Little & Hancock, 2002; Perrett et al., 1998; Rhodes, Hickford, & Jeffrey, 2000). That heterosexual, psychologically feminine men have more opposite-sex sexual partners (Zeitsch et al., 2008) would be consistent with this theory. Similarly, same-sex affiliation theory (Muscarella, 1999, 2000; Rahman & Wilson, 2003) suggests that ancestral men who were more feminine in behavior and who had bisexual preferences would be better adapted to cope with intergroup and intra-sex aggression (a factor in early hominid life, particularly for men) through same-sex affiliations. Additionally, these feminine characteristics would make the men more attractive to women as prospective fathers and partners, in both ways ultimately improving their fitness.
Alteration in methylation level at differential methylated regions of MEST and DLK1 in fetus of preeclampsia
Published in Hypertension in Pregnancy, 2018
Xiaoqing Wang, Liuxia Wan, Xiaoling Weng, Jiamin Xie, Aiping Zhang, Yun Liu, Minyue Dong
Also, human DLK1 is an imprinted gene located at chromosome 14q32 frequently showing uniparental disomy (UPD) and is imprinted and expressed from the paternal allele. This gene encodes a transmembrane protein named pre-adipocyte factor-1 (Pref-1) that contains multiple epidermal growth factor repeats that functions as a regulator of cell growth. Pref-1, an inhibitor of adipocyte differentiation, is increased in fetal blood of small for gestational age (SGA) and is considered a factor determining adiposity and associated with high risk of metabolic diseases in adulthood (41). A single nucleotide variant in this gene is associated with obesity in childhood and adolescence and shows polar overdominance, where heterozygotes carrying an active paternal allele expressing the phenotype, while mutant homozygotes are normal. It is indicated that DLK1 is related to adipose and muscle tissue development (42). Recently, increased serum Pref-1 was demonstrated in fetuses of preeclampsia-complicated pregnancy, and it may be a possible mediator leading to high risk of metabolic diseases in adulthood (43).
Confounds, Causality, and Sexual Orientation: The Implications of a Population-Level Study of Sibling Characteristics and Same-Sex Attraction
Published in The Journal of Sex Research, 2022
Scott W. Semenyna, Francisco R. Gómez Jiménez, Paul L. Vasey
The same is not true for the FFE—or as we prefer, the elevated reproduction predicted by the SAGH. The SAGH posits that certain genes result in androphilia when present in males (the causal mechanism) and increased fertility when present in females (Model B). The FFE is thus an indirect assay of the SAGH, and associations between male androphilia and the reproductive output of female relatives arise from this common cause. The SAGH is therefore both a proposed proximate explanation for male androphilia, as well as a potential ultimate explanation accounting for the continued existence of male androphilia in a population over evolutionary time via balancing selection. Both causal models predict an association between mothers’ reproduction and male androphilia, but they differ substantially in the mechanism involved. Model A proposes that a mother with high reproduction (for any reason) has a greater likelihood of having an androphilic son, and the relationship between mothers’ reproduction and a son’s androphilia is causally mediated through maternal immune response. Model B instead proposes that a genetic process causes a mother to have high reproduction, who in turn passes these genes on to her offspring, increasing the likelihood that a son will be androphilic.2Other genetic models for same-sex attraction have also been proposed, including overdominance (Zietsch et al., 2008), antagonistic pleiotropy (Zietsch et al., 2021), and polygenic effects (Ganna et al., 2019). These genetic effects could also be represented in diagrams like Figure 1, but the framing of the FFE discussed presently, and by Ablaza et al. (2021), is most strongly related to the SAGH. If model B is correct, the correlation between mothers’ reproduction, and a son’s androphilia, would be due to a common cause (i.e., sexually antagonistic genes). The empirical problem before us is determining which model best approximates reality, and whether past studies consistent with the SAGH, are instead only evidence of the FBOE (Blanchard et al., 2020b; Khovanova, 2020).