Corticosteroid signaling in frog metamorphosis

Kulkarni, Saurabh S.; Buchholz, Daniel R.

doi:10.1016/j.ygcen.2014.03.036

Cited by 34 publications

(22 citation statements)

References 73 publications

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“…Precisely timed hormonal cues mediate several crucial developmental transitions such as metamorphosis in invertebrates and amphibians (1, 2), molting in insects (3, 4), and growth and puberty in mammals (2, 5, 6). During mouse prostate ductal development, precisely timed androgenic cues guide a series of morphogenetic events that include prostatic bud specification (15–16 days post coitus, dpc), initiation (16–18 dpc), elongation (18+ dpc), and branching morphogenesis (birth-postnatal day 15) (7, 8).…”

Section: Introductionmentioning

confidence: 99%

Androgen receptor DNA methylation regulates the timing and androgen sensitivity of mouse prostate ductal development

Keil

Abler

Laporta

et al. 2014

Developmental Biology

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Androgen receptor (AR) signaling initiates mouse prostate development by stimulating prostate ductal bud formation and specifying bud patterns. Curiously, however, prostatic bud initiation lags behind the onset of gonadal testosterone synthesis by about three days. This study’s objective was to test the hypothesis that DNA methylation controls the timing and scope of prostate ductal development by regulating Ar expression in the urogenital sinus (UGS) from which the prostate derives. We determined that Ar DNA methylation decreases in UGS mesenchyme during prostate bud formation in vivo and that this change correlates with decreased DNA methyltransferase expression in the same cell population during the same time period. To examine the role of DNA methylation in prostate development, fetal UGSs were grown in serum-free medium and 5 alpha dihydrotestosterone (DHT) and the DNA methylation inhibitor 5’-aza-2’-deoxycytidine (5AzadC) were introduced into the medium at specific times. As a measure of prostate development, in situ hybridization was used to visualize and count Nkx3-1 mRNA positive prostatic buds. We determined that inhibiting DNA methylation when prostatic buds are being specified, accelerates the onset of prostatic bud development, increases bud number, and sensitizes the budding response to androgens. Inhibition of DNA methylation also reduces Ar DNA methylation in UGS explants and increases Ar mRNA and protein in UGS mesenchyme and epithelium. Together, these results support a novel mechanism whereby Ar DNA methylation regulates UGS androgen sensitivity to control the rate and number of prostatic buds formed, thereby establishing a developmental checkpoint.

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Section: Introductionmentioning

confidence: 99%

Androgen receptor DNA methylation regulates the timing and androgen sensitivity of mouse prostate ductal development

Keil

Abler

Laporta

et al. 2014

Developmental Biology

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“…Numerous studies have examined the effects of single chemical, complex chemical mixtures, or environmental exposures on amphibian morphology during metamorphosis and we focus our discussion on those that have additionally demonstrated a TH-dependence of these effects. Adverse toxicant and environmental exposures can compromise other endocrine and molecular signaling pathways beyond TH, with sub-lethal physiological consequences for reproductive success, behavior, and broader dysfunction (16–19). We have restricted our discussion to select representatives from each of the major classes listed above and regret being unable to undertake an exhaustive review of all the excellent work done on TH disruptors.…”

Section: Introductionmentioning

confidence: 99%

Contaminant and Environmental Influences on Thyroid Hormone Action in Amphibian Metamorphosis

et al. 2019

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Aquatic and terrestrial environments are increasingly contaminated by anthropogenic sources that include pharmaceuticals, personal care products, and industrial and agricultural chemicals (i. e., pesticides). Many of these substances have the potential to disrupt endocrine function, yet their effect on thyroid hormone (TH) action has garnered relatively little attention. Anuran postembryonic metamorphosis is strictly dependent on TH and perturbation of this process can serve as a sensitive barometer for the detection and mechanistic elucidation of TH disrupting activities of chemical contaminants and their complex mixtures. The ecological threats posed by these contaminants are further exacerbated by changing environmental conditions such as temperature, photoperiod, pond drying, food restriction, and ultraviolet radiation. We review the current knowledge of several chemical and environmental factors that disrupt TH-dependent metamorphosis in amphibian tadpoles as assessed by morphological, thyroid histology, behavioral, and molecular endpoints. Although the molecular mechanisms for TH disruption have yet to be determined for many chemical and environmental factors, several affect TH synthesis, transport or metabolism with subsequent downstream effects. As molecular dysfunction typically precedes phenotypic or histological pathologies, sensitive assays that detect changes in transcript, protein, or metabolite abundance are indispensable for the timely detection of TH disruption. The emergence and application of ‘omics techniques—genomics, transcriptomics, proteomics, metabolomics, and epigenomics—on metamorphosing tadpoles are powerful emerging assets for the rapid, proxy assessment of toxicant or environmental damage for all vertebrates including humans. Moreover, these highly informative ‘omics techniques will complement morphological, behavioral, and histological assessments, thereby providing a comprehensive understanding of how TH-dependent signal disruption is propagated by environmental contaminants and factors.

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“…In anurans, the effects of environmental stressors and elevated glucocorticoids on life history traits can differ depending on larval stage (Kulkarni & Buchholz, 2014; Wright et al, 1994). CORT slows down development in premetamorphosis, but accelerates development in prometamorphosis (Belden et al, 2005; Frieden & Naile, 1955; Gray & Janssens, 1990; Hu et al, 2008; Kikuyama et al, 1983; Kobayashi, 1958).…”

Section: Discussionmentioning

confidence: 99%

“…Beginning on May 31, 2016, mesocosms received their assigned treatment at night once every 2 weeks until September 18, when the dosing interval was increased to every 3 days. This design purposefully biased CORT exposure to larger larvae in later stages in development because CORT exposure in early development stages (when circulating thyroid hormones are low) is known to slow developmental progress and delay metamorphosis in anurans (Kulkarni & Buchholz, 2014; Wright et al, 1994). The design was also intended to reflect acute “stress” events such as antagonistic encounters with congeners or conspecifics, predator attacks or disturbance, hunger, or diurnal heat stress, wherein larval CORT levels increase but then return to basal levels through negative feedback of the HPI axis (Romero, 2004).…”

Section: Methodsmentioning

confidence: 99%

Exposure to glucocorticoids alters life history strategies in a facultatively paedomorphic salamander

2021

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Polyphenisms, where two or more alternative, environmentally‐cued phenotypes are produced from the same genotype, arise through variability in the developmental rate and timing of phenotypic traits. Many of these developmental processes are controlled or influenced by endogenous hormones, such as glucocorticoids, which are known to regulate a wide array of vertebrate ontogenetic transitions. Using the mole salamander, Ambystoma talpoideum, as a model, we investigated the role of glucocorticoids in regulating facultative paedomorphosis, an ontogenetic polyphenism where individuals may delay metamorphosis into terrestrial adults. Instead, individuals reproduce as aquatic paedomorphic adults. Paedomorphosis often occurs when aquatic conditions remain favorable, while metamorphosis typically occurs in response to deteriorating or “stressful” aquatic conditions. Since glucocorticoids are central to the vertebrate stress response and are known to play a central role in regulating obligate metamorphosis in amphibians, we hypothesized that they are key regulators of paedomorphic life history strategies. To test this hypothesis, we compared development of larvae in outdoor mesocosms exposed to Low, Medium, and High exogenous doses of corticosterone (CORT). Results revealed that body size and the proportion of paedomorphs were both inversely proportional to exogenous CORT doses and whole‐body CORT content. Consistent with known effects of CORT on obligate metamorphosis in amphibians, our results link glucocorticoids to ontogenetic transitions in facultatively paedomorphic salamanders. We discuss our results in the context of theoretical models and the suite of environmental cues known to influence facultative paedomorphosis.

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Corticosteroid signaling in frog metamorphosis

Cited by 34 publications

References 73 publications

Androgen receptor DNA methylation regulates the timing and androgen sensitivity of mouse prostate ductal development

Androgen receptor DNA methylation regulates the timing and androgen sensitivity of mouse prostate ductal development

Contaminant and Environmental Influences on Thyroid Hormone Action in Amphibian Metamorphosis

Exposure to glucocorticoids alters life history strategies in a facultatively paedomorphic salamander

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