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#chick embryo

43 public questions tagged with this topic.

Limb Development -ll

What happens when FGF10 beads are implanted in the flank of a chick embryo?

Classic sufficiency test placed FGF10 beads into interlimb flank where normally no limb forms due to absence of Tbx expression and inhibitory cues. Ectopic FGF10 activated FGFR2b, beta-catenin and induced a new AER expressing FGF8 and Wnt3a, initiating progress zone proliferation and complete supernumerary limb containing all three segments stylopod zeugopod autopod and digits with dorsal-ventral polarity. This demonstrated FGF10 as potent limb inducer and sufficient for de novo limb initiation, distinct from inhibition of growth, dorsalization of mesenchyme or homeotic transformation of forel

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: Ectopic FGF10 causes extra limb induction.

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chick development-l

Cerberus protein on the left side of chick embryos activates:

At stage when left-right asymmetry established, Sonic hedgehog expressed left of Hensen's node induces Cerberus-related Caronte in left paraxial and lateral plate mesoderm. Caronte functions as high-affinity BMP antagonist binding BMP2, BMP4, BMP7 extracellularly, preventing Smad1/5/8 phosphorylation that normally represses Nodal promoter via interplay with FoxH1 and Smad2. BMP inhibition lifts repression permitting Nodal autoactivation left side, followed by Lefty and Pitx2 expression directing asymmetric organ morphogenesis. Right side lacking Caronte maintains BMP blocking Nodal, explaining

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Cerberus activates Nodal via BMP inhibition in left-right patterning.

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chick development-l

Hensen’s node transplantation experiments result in:

Classic organizer experiment by Waddington grafted Hensen's node from donor chick embryo into lateral area pellucida of host embryo. Donor node retained autonomy expressing Chordin, Noggin, Shh and Goosecoid, antagonizing BMP in surrounding host epiblast inducing ectopic neural plate marked Sox2 and ectopic notochord. Host developed secondary embryonic axis complete with somites and neural tube parallel to primary axis. Result proved avian node equivalent to Spemann organizer, capable of neural induction and dorsal mesoderm patterning, demonstrating conserved mechanism of secondary axis induct

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Hensen's node transplantation inducing secondary embryonic axis.

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chick development-l

The anterior-posterior axis formation in chick embryos depends on:

Avian egg undergoes rotation within oviduct during albumen deposition and within shell due to chalazae twisting, generating fluid shear and gravitational cues. Experimental tilting of eggs before primitive streak formation shifts site of Koller's sickle activation and streak origin, indicating gravity-sensitive ionic and pH gradients bias Wnt and Vg1 localization posteriorly. Albumen pressure and blastoderm tension amplify asymmetry. Unlike amphibian sperm entry point, chick anterior-posterior specification relies on extraembryonic mechanical cues and gravity during rotation, later reinforced

Ref: Wolpert, Principles of Development, Chapter 4: Gravity and egg rotation in avian anterior-posterior axis formation.

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chick development-l

The chick extraembryonic membrane for waste storage and gas exchange is:

Allantois evaginates as endodermal diverticulum from embryonic hindgut surrounded by splanchnic mesoderm, protruding into extraembryonic coelom during day three incubation. Its mesoderm becomes highly vascularized via VEGF signaling, fusing with chorion forming chorioallantoic membrane where fetal vessels appose shell pores for respiratory gas exchange. Distal sac accumulates nitrogenous waste as insoluble uric acid since embryo cannot excrete via yolk. Thus single membrane serves dual physiological roles: waste storage and breathing organ, expanding to occupy most coelom, later contributing t

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Allantois - waste storage and gas exchange extraembryonic membrane.

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chick development-l

Hensen’s node contains cells destined to become:

Lineage analysis of Hensen's node using quail-chick chimeras reveals median pit cells ingress after streak regression to form notochordal rod extending caudally, expressing Brachyury, FoxA2 and Sonic hedgehog providing signals for ventral neural tube and somite patterning. Lateral and rostral node cells contribute prechordal mesendoderm underlying forebrain, expressing Goosecoid, Otx2 and Hex, crucial for head induction and forebrain specification by inhibiting Wnt and BMP. Together axial progenitors provide structural scaffold and signaling center for body plan, not limb or epidermal derivati

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Hensen's node progenitors - notochord and prechordal mesoderm formation.

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chick development-l

If FGF signaling is artificially activated in chick, the primitive streak orientation:

Normal FGF4 expressed posteriorly maintains Wnt8c domain and primitive streak position by suppressing anterior streak genes. Experimental application of exogenous FGF8 beads or FGF-soaked grafts to anterior marginal zone reprograms epiblast competence, inducing ectopic Brachyury and repressing endogenous posterior streak via inhibitory feedback loop involving Sprouty and BMP antagonists. Because epiblast remains plastic early, gradient reversal relocates Nodal signaling and streak now initiates anteriorly extending posteriorly, effectively reversing orientation of embryonic axis. Demonstrates

Ref: Wolpert, Principles of Development, 5th ed., Chapter 5: FGF artificial activation reversing primitive streak orientation experiments.

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chick development-l

Primitive streak migration in chick is regulated by:

Primitive streak extension requires coordinated convergence-extension driven by planar cell polarity Wnt pathway activating Dishevelled, RhoA and JNK, orienting mediolateral intercalation of epiblast cells toward posterior midline. Simultaneously FGF signaling through FGFR1 and MAPK ERK maintains Brachyury expression, cell motility and EMT via Snail2. Inhibition of FGFR or Wnt5a/Wnt8c perturbs streak elongation, causes premature regression or randomization. BMP inhibition anteriorly via Cerberus confines streak posteriorly. This integrated Wnt-PCP and FGF module conserved across vertebrates re

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Wnt/PCP and FGF regulation of primitive streak migration.

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chick development-l

Cells ingressing through posterior primitive streak in chick form:

Fate mapping using DiI labeling of chick primitive streak reveals anterior-posterior regionalization: Hensen's node contributes notochord and prechordal plate head mesoderm expressing Goosecoid, anterior streak forms paraxial somitic mesoderm, middle forms intermediate mesoderm, posterior streak contributes lateral plate and extraembryonic mesoderm. Posterior epiblast exposed to high BMP4 and Wnt8 signals activates lateral plate markers FoxF1 and promotes vascularization. Posterior ingressing cells split into somatic and splanchnic layers generating body wall, limbs and yolk sac vasculature gu

Ref: Wolpert, Principles of Development, 5th ed., Chapter 5: Posterior primitive streak forming lateral plate mesoderm fate.

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chick development-l

Formation of the blastocoel-like cavity in chick occurs between:

Chick blastoderm initially bilaminar with dorsal epiblast epithelium and ventral hypoblast layer of polyingressed cells. Subgerminal cavity appears between them through fluid secretion by epiblast via Na-K-ATPase transport, lifting blastoderm off yolk. This space considered blastocoel-like cavity, homologous to amphibian blastocoel though not fully enclosed. It permits hypoblast migration and later mesoderm spreading after ingression through primitive streak. Cavity roof is epiblast, floor hypoblast, not between hypoblast layers. Definitive endoderm ingressing through streak eventually obliter

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Blastocoel-like cavity formation between epiblast and hypoblast.

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chick development-l

The primary role of yolk sac in chick embryos is:

Yolk sac in chick originates from splanchnopleure consisting of definitive endoderm derived from primitive streak ingression plus splanchnic lateral plate mesoderm spreading over massive yolk mass, developing extensive vitelline vasculature. Endodermal cells express cathepsins and lipases endocytosing lipoprotein yolk platelets, hydrolyzing triglycerides and vitellogenin, transferring amino acids, lipids, iron and vitamins into embryonic bloodstream. Although chorioallantois later handles gas exchange, yolk sac remains primary nutritional organ throughout incubation and early hematopoietic sit

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 12: Yolk sac as nutritive extraembryonic membrane in birds.

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chick development-l

The dorsal-ventral axis in chick embryos is determined by:

Early chick axis establishment involves subtle bioelectric differences rather than simple genetic prepattern alone. Measurements show posterior marginal cells exhibit distinct intracellular pH elevation and depolarized membrane potential regulating beta-catenin nuclear transport and Vg1 exocytosis. These electrochemical gradients influenced by gravity during egg rotation in albumen and shell create biased Wnt8c and Nodal expression posteriorly. Subsequent feedback through Wnt, FGF and TGF-beta reinforces dorsoventral and anteroposterior polarity. While genes elaborate pattern, initial bias lin

Ref: Gilbert, Developmental Biology, 11th ed., Chapter 12: Chick axis specification - pH, membrane potential and gravity influences.

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