Tercera semana de desarrollo embrionario

Scientific concepts / nature phenomena covered (3rd week of embryonic development)

Gastrulation and the formation of germ layers

Key event: gastrulation

Gastrulation establishes the three germ layers (“from the outside in”):

• Ectoderm
• Intra-/intraembryonic mesoderm
  • The text distinguishes intraembryonic vs extraembryonic mesoderm.
• Endoderm

Primitive streak formation

• Gastrulation begins with the formation of the primitive streak in a groove.
• Primitive node: a cephalic, slightly raised region surrounding the primitive pit.

Cell movements

• Epiblast cells migrate toward the primitive streak and insert between the epiblast and hypoblast.
• Some cells intercalate with the hypoblast.
• Cell movement is described as invagination, guided by growth factors.

Role of growth factors / cadherins

• FGF is mentioned, specifically FGF8.
• FGF signaling leads to decreased cadherin, a protein that normally holds epiblast cells together—allowing migration.

Formation of mesoderm and endoderm

• Cells that remain in the epiblast become ectoderm.
• The newly formed layer created by migrating/intercalating cells becomes intraembryonic mesoderm (mesoderm within the embryo proper).
• Interaction between epiblast and hypoblast causes naming change such that the interposed/displaced layer is described as endoderm.
• Result: a trilaminar germ disc consisting of ectoderm–mesoderm–endoderm.

Notochord (notochord) and neural induction

Prechordal plate

• Later forms the buccopharyngeal membrane (described as occurring in a “subsequent” anterior timing).

Notochordal plate → notochord

• Epiblast cells migrate from the primitive node → prechordal plate to form the notochordal plate, embedded in endoderm.
• The plate differentiates and elongates into the notochord, extending cephalic to caudal.

Downstream inductions

• The notochord induces neural plate formation, which forms the neural tube.
• The notochord also contributes to formation of vertebral bodies.

Buccopharyngeal and cloacal membranes

Buccopharyngeal membrane

• Formed in the caudal/anterior region described via the prechordal plate.

Cloacal membrane

• Formed similarly in the caudal region of the embryonic disc.

Tissue composition rule (explicitly stated)

• Both membranes are formed only by ectoderm and endoderm.

Allantois and neuroenteric duct (extraembryonic derivatives)

Allantois (enteric diverticulum)

• Appears around day ~16.
• Induces formation of umbilical vessels.
• Mentioned involvement in bladder developmental anomalies.

Umbilical cord

• Umbilical blood vessels + connective tissue film later contribute to the future umbilical cord.

Neuroenteric duct

• Temporarily connects the amniotic cavity with the yolk sac when the primitive pit forms a notch.

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Establishment of body axes (timing, patterning genes)

Anteroposterior (head–tail) axis

• Established before and during gastrulation.

Anterior visceral endoderm

• Expresses genes important for head formation, including:
  • OTX2, LM1, HX1
• Includes factors secreted by Cerberus and Lefty.

Nodal gene

• Expressed/regulated in relation to these factors.
• Important for:
  • Maintenance/formation of the primitive streak
  • Regulating numbers of mesoderm-related genes and tail/head structures.

HNF3β (Hepatocyte nuclear factor 3 beta)

• Maintains the primitive node.
• If absent → gastrulation fails and missing regions such as:
  • prosencephalon
  • mesencephalon
• The text states HNF3β specifies these regions.

Mesoderm subdivisions and their fates

Mesoderm is described as having three parts:

• Paraxial mesoderm
  • Forms muscles, mesentery, and other derivatives.
• Intermediate mesoderm (urogenital mesoderm)
  • Forms kidneys and contributes to the urinary system.
• Lateral plate mesoderm
  • Forms blood and the body wall.

Gene/growth-factor-mediated displacement of mesoderm

The text references multiple regulators that shift mesodermal fate/position:

• Chordin and noggin (also written in the text as misread variants)
• Follistatin (written as “folaa” in the text)
  • Inhibit SE4 morphogenetic protein (likely a BMP-related term error in the notes)
  • Shift mesoderm toward anterior/cephalic regions.
• FGF + morphogenetic protein 4
  • Displaces intermediate and lateral plate mesoderm toward the sides of paraxial mesoderm.
• A gene labeled “bruri or hent”
  • Drives formation of central/caudal mesoderm
  • Absence causes caudal dysgenesis.

Left–right laterality (asymmetry)

Left–right asymmetry is determined by a gene cascade:

1. Primitive node expresses FGF8
2. FGF8 establishes NODAL expression
3. NODAL accumulates on the left side
4. After neural tube formation:
   • FGF8 induces expression of NODAL and lecti2 (likely Lefty2)
   • These regulate PITX2

Serotonin (5-HT) involvement

• The cascade depends on 5-HT (serotonin) concentration:
  • Concentration increases on the left.
• Asymmetric mechanisms mentioned:
  • MAO (monoamine oxidase) degrades serotonin and prevents left-side gene expression on the right.
  • A right-side barrier involving Shh (“Sonic sounds… shh”) and a factor labeled G prevents left-side genes from being expressed on the right.

Alterations noted

• “Reverse cardiomyopathy” and heart conditions are mentioned as linked to changes (the text contains confusing/possibly misrecognized phrases related to serotonin).

Right-sided determination

• Not well defined in the text.
• SILE factor/gene is mentioned as responsible for right-handedness.

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Researchers / sources featured

• No specific researchers are named as people.
• Named biological factors include:
  • FGF8
  • OTX2, LM1, HX1
  • Cerberus
  • Lefty (written as “Leftii/Leftii”)
  • NODAL
  • HNF3β
  • Chordin, noggin, follistatin (written as “folaa”)
  • BMP / morphogenetic protein 4 (written as “morphogenetic protein 4”)
  • PITX2
  • 5-HT (serotonin), MAO
  • Shh
  • Lefty2 (written as “lecti2”)
  • SILE (right-handedness factor)