Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (682 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The developmental entity of a fertilized chicken egg (zygote). The developmental process begins about 24 h before the egg is laid at the blastodisc, a small whitish spot on the surface of the egg yolk. After 21 days of incubation, the embryo is fully developed before hatching.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Embryo, Chick; Chick Embryos; Embryos, Chick.
Where it fits in the MeSH classification
- Broader topics
- Embryo, Nonmammalian
Related concepts
- Zygote
- Blastodisc
- Egg Yolk
Research landscape
PubMed indexes 61,885 records tagged with the MeSH heading “Chick Embryo” (counts retrieved 2026-10-31). 2,659 of them (4.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 42,837 records.
Reviews account for 2,528 records (4.1%) and meta-analyses for 8. Randomized controlled trials number 72 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 42,837 |
| 2000-2009 | 9,448 |
| 2010-2019 | 6,941 |
| 2020 onward | 2,659 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,528 | 4.1% |
| Meta-analyses | 8 | 0.0% |
| Randomized controlled trials | 72 | 0.1% |
Method: PubMed query "Chick Embryo"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Limb proportions show developmental plasticity in response to embryo movement | 2017 | Research article Design not recorded in structured metadata | 1,314 | cc by PMID 28165010 · DOI · PMC5292730 |
| Embryonic exposure to corticosterone modifies the juvenile stress response, oxidative stress and telomere length | 2012 | Research article Design not recorded in structured metadata | 228 | cc by PMID 22072607 · DOI · PMC3282378 |
| FGF, Insulin, and SMAD Signaling Cooperate for Avian Primordial Germ Cell Self-Renewal | 2015 | Research article Design not recorded in structured metadata | 190 | cc by PMID 26677769 · DOI · PMC4682126 |
| Core microRNAs regulate neural crest delamination and condensation in the developing trigeminal ganglion | 2025 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41329730 · DOI · PMC12704738 |
Limb proportions show developmental plasticity in response to embryo movement [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Animals have evolved limb proportions adapted to different environments, but it is not yet clear to what extent these proportions are directly influenced by the environment during prenatal development.
- Closing excerpt
- Our findings provide new insights into how environmental factors can be integrated to influence cellular activity in growing bones and ultimately gross limb morphology, to generate phenotypic variation during prenatal development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Animals have evolved limb proportions adapted to different environments, but it is not yet clear to what extent these proportions are directly influenced by the environment during prenatal development. The developing skeleton experiences mechanical loading resulting from embryo movement. We tested the hypothesis that environmentally-induced changes in prenatal movement influence embryonic limb growth to alter proportions. We show that incubation temperature influences motility and limb bone growth in West African Dwarf crocodiles, producing altered limb proportions which may, influence post-hatching performance. Pharmacological immobilisation of embryonic chickens revealed that altered motility, independent of temperature, may underpin this growth regulation. Use of the chick also allowed us to merge histological, immunochemical and cell proliferation labelling studies to evaluate changes in growth plate organisation, and unbiased array profiling to identify specific cellular and transcriptional targets of embryo movement. This disclosed that movement alters limb proportions and regulates chondrocyte proliferation in only specific growth plates. This selective targeting is related to intrinsic mTOR (mechanistic target of rapamycin) pathway activity in individual growth plates. Our findings provide new insights into how environmental factors can be integrated to influence cellular activity in growing bones and ultimately gross limb morphology, to generate phenotypic variation during prenatal development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28165010 · DOI · PMC5292730
Embryonic exposure to corticosterone modifies the juvenile stress response, oxidative stress and telomere length [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Early embryonic exposure to maternal glucocorticoids can broadly impact physiology and behaviour across phylogenetically diverse taxa.
- Closing excerpt
- Given this, long-term costs of glucocorticoid-induced phenotypes may include accelerated ageing and increased mortality.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (197 words)
Early embryonic exposure to maternal glucocorticoids can broadly impact physiology and behaviour across phylogenetically diverse taxa. The transfer of maternal glucocorticoids to offspring may be an inevitable cost associated with poor environmental conditions, or serve as a maternal effect that alters offspring phenotype in preparation for a stressful environment. Regardless, maternal glucocorticoids are likely to have both costs and benefits that are paid and collected over different developmental time periods. We manipulated yolk corticosterone (cort) in domestic chickens (Gallus domesticus) to examine the potential impacts of embryonic exposure to maternal stress on the juvenile stress response and cellular ageing. Here, we report that juveniles exposed to experimentally increased cort in ovo had a protracted decline in cort during the recovery phase of the stress response. All birds, regardless of treatment group, shifted to oxidative stress during an acute stress response. In addition, embryonic exposure to cort resulted in higher levels of reactive oxygen metabolites and an over-representation of short telomeres compared with the control birds. In many species, individuals with higher levels of oxidative stress and shorter telomeres have the poorest survival prospects. Given this, long-term costs of glucocorticoid-induced phenotypes may include accelerated ageing and increased mortality.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22072607 · DOI · PMC3282378
FGF, Insulin, and SMAD Signaling Cooperate for Avian Primordial Germ Cell Self-Renewal [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Precise self-renewal of the germ cell lineage is fundamental to fertility and reproductive success.
- Closing excerpt
- These defined medium conditions identify the key molecular pathways required for PGC self-renewal and will facilitate efforts in biobanking of chicken genetic resources and genome editing.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
Precise self-renewal of the germ cell lineage is fundamental to fertility and reproductive success. The early precursors for the germ lineage, primordial germ cells (PGCs), survive and proliferate in several embryonic locations during their migration to the embryonic gonad. By elucidating the active signaling pathways in migratory PGCs in vivo, we were able to create culture conditions that recapitulate this embryonic germ cell environment. In defined medium conditions without feeder cells, the growth factors FGF2, insulin, and Activin A, signaling through their cognate-signaling pathways, were sufficient for self-renewal of germline-competent PGCs. Forced expression of constitutively active MEK1, AKT, and SMAD3 proteins could replace their respective upstream growth factors. Unexpectedly, we found that BMP4 could replace Activin A in non-clonal growth conditions. These defined medium conditions identify the key molecular pathways required for PGC self-renewal and will facilitate efforts in biobanking of chicken genetic resources and genome editing.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26677769 · DOI · PMC4682126
Core microRNAs regulate neural crest delamination and condensation in the developing trigeminal ganglion [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Cranial neural crest cells (NCCs) undergo dynamic processes during embryonic development, including delamination from the neural tube by epithelial-to-mesenchymal transition (EMT), migration to the periphery, condensation via mesenchymal-to-epithelial transition (MET), and differentiation into structures like the trigeminal ganglion.
- Closing excerpt
- Our findings shed light on the intricate regulatory networks governing NCC behavior, positioning miRNAs as key regulatory elements required for migratory transitions and axial level-specific differentiation capabilities.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (138 words)
Cranial neural crest cells (NCCs) undergo dynamic processes during embryonic development, including delamination from the neural tube by epithelial-to-mesenchymal transition (EMT), migration to the periphery, condensation via mesenchymal-to-epithelial transition (MET), and differentiation into structures like the trigeminal ganglion. Here, we identify and characterize the function of a core set of miRNAs involved in these transitions during the formation of the trigeminal ganglion in the chick embryo. We further identify putative targets of miRNAs involved in neural crest EMT and MET. Notably, introducing MET-involved miRNAs into trunk NCCs endows these cells with the ability to condense and differentiate into neurons in vivo in a manner reminiscent of cranial rather than trunk NCCs. Our findings shed light on the intricate regulatory networks governing NCC behavior, positioning miRNAs as key regulatory elements required for migratory transitions and axial level-specific differentiation capabilities.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41329730 · DOI · PMC12704738
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Early stages of chick somite development [5]
- Research article Developmental patterning of the myocardium [6]
- Research article In situ hybridization analysis of chick embryos in whole mount and tissue sections [7]
- Research article Manipulating gene expression with replication-competent retroviruses [8]
- Research article Lipid metabolism and the neonatal chicken [9]
- Research article Development of the vertebrate cornea [10]
References
- Pollard AS, Charlton BG, Hutchinson JR, Gustafsson T, McGonnell IM, Timmons JA, et al.. Limb proportions show developmental plasticity in response to embryo movement. . 2017. PMID 28165010 · DOI · PMC5292730
- Haussmann MF, Longenecker AS, Marchetto NM, Juliano SA, Bowden RM. Embryonic exposure to corticosterone modifies the juvenile stress response, oxidative stress and telomere length. . 2012. PMID 22072607 · DOI · PMC3282378
- Whyte J, Glover JD, Woodcock M, Brzeszczynska J, Taylor L, Sherman A, et al.. FGF, Insulin, and SMAD Signaling Cooperate for Avian Primordial Germ Cell Self-Renewal. . 2015. PMID 26677769 · DOI · PMC4682126
- Marquez RB, Sánchez Vásquez E, Alonso AM, Bernardi YE, Santillan EM, Lwigale P, et al.. Core microRNAs regulate neural crest delamination and condensation in the developing trigeminal ganglion. . 2025. PMID 41329730 · DOI · PMC12704738
- Christ B, Ordahl CP. Early stages of chick somite development. Anat Embryol (Berl). 1995. PMID 7625610 · DOI
- Sedmera D, Pexieder T, Vuillemin M, Thompson RP, Anderson RH. Developmental patterning of the myocardium. Anat Rec. 2000. PMID 10737851 · DOI
- Nieto MA, Patel K, Wilkinson DG. In situ hybridization analysis of chick embryos in whole mount and tissue sections. Methods Cell Biol. 1996. PMID 8722478 · DOI
- Morgan BA, Fekete DM. Manipulating gene expression with replication-competent retroviruses. Methods Cell Biol. 1996. PMID 8722477 · DOI
- Noble RC, Cocchi M. Lipid metabolism and the neonatal chicken. Prog Lipid Res. 1990. PMID 2093896 · DOI
- Hay ED. Development of the vertebrate cornea. Int Rev Cytol. 1980. PMID 395131 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.