This minireview summarizes the role of androgen signaling in sexually dimorphic development of the genital tubercle. Androgen signaling has been identified as the primary factor that establishes male characteristics. The ligands for androgen signaling are testosterone and dihydrotestosterone, and testosterone is the primary circulating androgen secreted by Leydig cells of the testis.

This review argues that hormones are proximate regulators of sex differences by mediating sex-biased trait expression. It notes that testosterone levels in males and females covary across species and can influence traits subject to selection, but it does not claim testosterone is the sole or principal mechanism for all sexual dimorphism.

In general, the establishment of phenotypic dimorphisms in rodents is generated by different levels of hormones at specific times in XX and XY individuals. Males have an early surge of testosterone, and females a later surge of estrogens. In sum, estrogens are described here as the ultimate agents of both female and male sexual differentiation in the brain.

“Individuals must attain the morphological and physiological ability to reproduce, a process that depends upon…gonadal sex determination, the subsequent development of the accessory sex structures (reproductive tract and genitalia), and the later maturation of the organism by pubertal hormones, leading to the development of secondary sex characteristics that distinguish males and females and serve as the basis for mate choice.” “Whereas gonadal sex determination is independent of sex hormones, development of the reproductive tract…occurs under the influence of gonadal steroid hormones in a sexually dimorphic manner.” “The differentiation of the male and female reproductive tracts occurs under the influence of anti-Müllerian hormone and testosterone.” “In brief, gonadal steroids, especially testosterone and estradiol, first organize the brain…During puberty, the increasing concentrations of gonadal steroid hormones also lead to the development of secondary sexual characteristics…These characteristics play a vital role in sexual selection since they are used as visual indicators of mate quality.”

In males it is frequently testosterone that activates the expression of sexually selected morphological and behavioral displays. We show that females have the capacity to express most male-typical traits in response to exogenous testosterone, including carotenoid-pigmented body plumage, shorter feathers, darkened bill and enlarged cloacal protuberance. Low androgen levels during the pre-nuptial molt prevent females from developing male-like ornamentation.

The article states that sexual dimorphism arises in part from sex differences in gene expression and that steroid hormones are often invoked as a proximate cause of sexual dimorphism. It also says testosterone regulates several sexually dimorphic phenotypes, including sexual signals, aggression, breeding state, and courtship behavior.

It is widely assumed that the development of male secondary sexual traits in birds and mammals is testosterone-dependent. Male-specific behaviors and physical traits, like spurs and wattles, are typically influenced by testosterone levels. Nonetheless, in birds, masculine plumage can arise from distinct mechanisms, and not all sexually dimorphic traits are directly testosterone-dependent.

Sex-biased regulation of genes via sex hormone signaling offers an intuitive mechanism by which males and females could develop different body sizes. Since males and females share most of their genome, sexual size dimorphism must arise from sex-specific regulation of the genome, for example via changes in the number of sites in the genome that bind sex hormone receptors. Across 268 mammal species with complete genomes, we find that species with the highest sexual size dimorphism (male-larger) tend to harbor more androgen binding elements near genes, but only in small-bodied lineages. While it is not yet possible to definitively assign differences in body size to genome-wide molecular mechanisms, our study suggests that hormonal signaling is an important mechanism for small-bodied species to achieve SSD relatively quickly.

“Testosterone is the principal androgen responsible for male sex differentiation, development of male secondary sexual characteristics, spermatogenesis, libido, and overall male fertility.” “Testosterone drives primary male sexual development, including testicular descent, enlargement of the penis and testes…Testosterone is a primary regulator of secondary male sexual characteristics—the features associated with phenotypic masculinity.” “These features include male-pattern body and facial hair growth, deepening of the voice…Testosterone exerts anabolic effects as well, driving the pubertal growth spurt…”

This review reports that testosterone is a key hormone for the development of secondary sexual characters and dimorphisms in behavior and morphology of male vertebrates. It also summarizes comparative evidence that male-to-female testosterone ratios are associated with the degree of sexual dimorphism in birds and fish.

We tested whether evolutionary shifts in the direction of sexual size dimorphism correspond to underlying changes in the endocrine regulation of growth. Castration inhibits, and testosterone stimulates, male growth. These studies reveal that the evolution of sexual size dimorphism has been accompanied by underlying changes in the effect of testosterone on male growth.

The presence of sexually selected traits in males was significantly correlated with increased peak androgen levels in males as well as females, and female peak androgen levels were significantly higher in species where females expressed male-like sexually selected traits. These results support the hypothesis that androgens are an important endocrine mechanism influencing the expression of sexually selected traits in both sexes. However, they also suggest that endocrine constraints may limit the extent to which sexual selection can drive dimorphism, because shared hormonal regulation can couple trait expression between males and females.

“Testosterone can activate the androgen receptor itself or after conversion to 5α-dihydrotestosterone (DHT)…Testosterone is the principle male sex hormone in mammals, birds and other vertebrates.” “A deficiency in the enzyme 5-alpha reductase…reduces the androgenic effects responsible for male development before birth and during puberty. The shortage of DHT prevents proper formation of the male sex organs…” “Testosterone also promotes the secondary sexual characteristics in males during puberty such as increased muscle mass, increased bone mass, deepening of the voice and the growth of facial, armpit, chest and pubic hair.”

The results in males strongly suggest that masculinization by male gonadal androgens during growth is not required for the development of sexual dimorphism in body size and casque size in the chameleon. In some squamates, many male-typical exaggerated traits including body size were assumed to be controlled by masculinization by male gonadal androgens. However, exogenous androgens in females can lead to male-typical growth via interference with normal hormonal secretion of ovaries and hence causing defeminisation, rather than masculinization presuming the direct effect of androgens on growth. The ontogeny of sexually dimorphic body size and exaggerated traits in at least some squamates is likely controlled by other proximate mechanisms, possibly by feminization by ovarian hormones.

“Overall, effects of sexuality on T across species highlight the malleability of androgens, particularly in response to the social environment.” “In particular, testosterone (T) is implicated in tradeoffs relevant to life-history strategies, such that high T is linked with competition (i.e., acquisition or defense of resources, including sexual partners or opportunities) and low T is linked with nurturance…” “Behaviorally, T promotes competition for resources, including sexual partners, territories, and status…In some species, T increases locomotor activity and risk-taking behavior, which can facilitate sexual and territorial competition…”

Testosterone contributes significantly to the sexual development, appearance and aggression behavior of males. To exert its function, testosterone binds to the androgen receptor, which then triggers the production of specific proteins in the cell. The article also emphasizes that testosterone is important in both sexes and that its effects are not exclusive to males.

“Testosterone is the primary male sex hormone and androgen in males.” “In humans, testosterone drives the development of male reproductive tissues such as testicles and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair.” “Specifically, testosterone, along with anti-Müllerian hormone (AMH) promote growth of the Wolffian duct and degeneration of the Müllerian duct respectively. This period affects the femininization or masculinization of the fetus…” “The effects of testosterone…occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as dihydrotestosterone), and by conversion to estradiol and activation of certain estrogen receptors.”

Sexual dimorphism is the condition where different sexes of the same species exhibit different morphological characteristics. One explanation is that endocrinological differences between the sexes impact the immune system, and testosterone acts as an immunosuppressive agent. Darwin linked sexual dimorphism to sexual selection.

“Male sexual development and hormonal function depend on a complex feedback circuit involving the hypothalamus-pituitary-gonadal (HPG) axis…” “Testosterone, DHT, and estradiol provide negative feedback on the hypothalamic-pituitary axis.” “In males, estradiol is the main inhibitor of LH production, whereas both estradiol and inhibin B…inhibit production of FSH.” This section highlights that multiple sex steroids (testosterone, its metabolite DHT, and estradiol) are involved in regulating male reproductive endocrinology rather than testosterone acting alone.

“Testosterone (T) mediates a variety of traits that function in competition for mates, including territorial aggression, ornaments, armaments, and gamete production.” “Across many taxa, T has been proposed as a key physiological mediator of trade-offs between investment in mating and parental effort.” The study emphasizes that T is an important mediator of sexually selected traits and behaviors but examines its variation in a sex- and stage-specific manner, implying that its role is context dependent and interacts with other factors.

In males, it is typically testosterone (T) that activates secondary sex characters such as sexually selected behavioral and ornamental traits. In this study, we demonstrate that experimentally elevating T in females activates male-typical sexual dimorphism in growth, plumage, and song. Our findings suggest that T can act as a proximate endocrine mechanism by which sexual selection translates into sex differences in morphology and behavior when the underlying genetic architecture is shared between males and females.

“Testosterone regulates its production through negative feedback mechanisms, with high levels of this hormone suppressing GnRH and gonadotropins release.” “In adult men, testosterone is mainly secreted by testicular Leydig cells under LH stimulation, while the adrenal glands also contribute…” The review focuses on secular trends in testosterone but underscores its central role as a gonadal steroid while also treating it as part of a broader endocrine network that includes GnRH, LH, FSH, adrenal androgens and other hormones.

The preprint states that humans are sexually dimorphic and that these differences are likely mediated in part by developmental testosterone. It also frames testosterone as one of several traits associated with mating outcomes, not as the sole principal mechanism linking sexual selection to morphology.

“Despite a common belief that testosterone regulates fluctuations in human sexual desire, there is little direct evidence that relates within-person variation in testosterone to within-person variation in desire.” “We found little evidence that day-to-day changes in testosterone were associated with changes in solitary or partnered sexual desire for men or women.” Although focused on sexual desire rather than morphology, this paper illustrates that testosterone is not always the sole or dominant endocrine mechanism even for sexual traits traditionally assumed to be T-driven.

Sex-limited secretion of hormones is one mechanism that can transiently activate or permanently organize sexually dimorphic characters. This provides a framework for understanding how hormone signaling can translate sex differences into trait differences.

Sexual dimorphism is the term used to describe when the two sexes of a species possess physical characteristics that differ from each other. These differences can include coloration, body size, ornamentation, or other morphological traits, and they often arise through sexual selection, natural selection, or a combination of selective pressures. Hormones such as testosterone and estrogen are frequently involved in the development of secondary sexual characteristics, but the exact mechanisms can vary widely among taxa.

This chapter is about sexual selection, measures of sexual selection, and sexual dimorphism in primates. It is relevant background for the claim, but the available search result does not provide a specific passage linking testosterone to the principal mechanism by which sexual selection produces morphological dimorphism.

This chapter reviews how sex steroids, including testosterone, function as proximate mechanisms underlying sexual dimorphism in vertebrates. It emphasizes that while androgens often regulate male-typical traits such as larger body size, weapons, or ornaments, sexual dimorphism can also arise through sex-specific sensitivity of tissues to hormones, local conversion of hormones, and differences in female hormones such as estrogens. Thus, testosterone is an important but not exclusive endocrine mechanism linking sexual selection to morphological divergence between the sexes.

This review says sexual selection theory predicts that males competing for mates may evolve larger body size and other traits, but the search result excerpt provided does not specifically establish testosterone as the principal endocrine mechanism translating sexual selection into morphological sexual dimorphism.