LECTURE 2: General Embryology II (NYUCD)

Somatic cells
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- A process characterized by profound cell movements that convert a sheet of cells into a multi-layered
*Bilaminar group of cells --> Multilayer organisms

-One of consequences of this reorganization is that group of cells are brought in close contact to
undergo inductive interactions.
*Group of cells at a distance will come close in apposition
> give rise to a lot of cells of the three germ layers

-Groove in which cells will invaginate into cavity

*Cells move into cavity (epithelium into mesenchymal transition)
*Loose contact with enveloping cells and fold and enter cavity during the process
*Cells will migrate from each site of the primitive streak and from the primitive node
Image: Primitive streak
- Epiblast cells forming the primitive streak migrate in an anterior position to form the node.

- First cells passing through the primitive streak displace the cells of the hypoblast to give rise to the
embryonic/definitive endoderm.

- Cells at the node move anteriorly to form the head mesoderm and the notochord as the primitive
streak regresses.

- Cells moving through the primitive streak between the epiblast and the endoderm will form the
embryonic mesoderm.

- Epiblast cells that remain at the surface will form the embryonic ectoderm.

- ECTODERM AND ENDODERM: derived from epiblast

- MESODERM: axon of the notochord
Neural Inductionthe process by which neural plate is generated >Gastrulation: allow mesoderm to migrate right underneath ectoderm --> allow for inductive interaction to take placeInductive interaction between the chordamesoderm/notochord and the ectodermSignal derived from tissue induces the overlaying ectoderm to form neural plateMolecular Regulation of Neural Induction-The secreted molecule bone morphogenetic protein 4 (BMP4) expressed throughout the ectoderm regulates the decision between epidermal and neural fate * BMP4: promotes bone growthBMP4NO INHIBITION ectoderm into dermis - regulates the decision between epidermal and neural fate and it promotes bone growth - BMP4 will bind to its receptor, activated/secreted by ectoderm --> epidermal ectodermInhibition of BMP4ECTODERM into (anterior) neural plate or FOREBRAIN Inhibition of BMP4 signaling in the ectoderm is required to convert the ectoderm into neural tissue (mediated by the dorsal mesoderm)BMP4 antagonists- Noggin, Chordin and Follistatin - Are secreted by the dorsal mesoderm/notochord - They bind BMP4 molecules preventing BMP4 interaction with its receptorBMP4 antagonists + FGF/RETINOIC ACID/Wnt-3A(1) ACTIVATION: mesoderm secrete caudal antagonist (chordin, noggin, follstatin) (2) TRANSFORMATION: FGF, retinoic acid and Wnt-3a --> transformation of (posterior) neural plate = neural tube (pattern neural tissue from anterior-posterior)ACTIVATION:mesoderm secrete caudal antagonist (nogging, chordin, and follistatin)TRANSFORMATION:FGF, retinoic acid and Wnt-3a --> transformation of neural tissue with anterior-posterior character (pattern neural tissue from anterior-posterior)NeurulationThe process by which the neural plate folds into the neural tube.Neurulation results in the segregation of:the three ectodermal derivatives: -neural tube *(CNS-brain) -neural crest -epidermis (outer ectoderm)shaping:thickening of cells that form neural platefolding:neural plate starts to foldelevation:fold of neural plate starts to rise upclosure:tip of neural plate will fuse together DORSALLYconvergence:the tips will come togetherNeural plates starts "zipping" up/down atthe MIDBRAIN@ 19 days:- Open neural plate - Remaining primitive streak@ 20 days:Neural Plate forms in middle of embryo and then closes up as zipper going in both directions@ 22 days:neural tube opened at posteriorally end of embryo but closed at anterior end@ 23 days:Almost close only open at the endsNeural tube closure in chickis initiated at the level of the future midbrain and "zips up" in both directions.Caudal neuroporesare the last regions to close are the large openings at either end of the neural tubeNeural Tube Closure Defects- occur in the most cranial and caudal regions because they are the last to close - are caused when various part of the neural tube fail to close. **are among the most common congenital anomalies**Failure to close the neural tubeoccurs most frequently in the cranial and the caudal regions.AnencephalyFailure to close the anterior neural tube regions. (forebrain remains in contact with the amniotic fluid and degenerates)Spina BifidaFailure to close the neural tube in the caudal region -The severity of which depends on how much of the spinal cord remains exposed. -The most severe cases of spina bifida involve protrusion of the spinal cord and meninges through the defective vertebral arches and other superficial structures (spina bifida cystica).Craniorachischisisopen brain and spinal cordNEURAL CREST DEVELOPMENT-developed from neural plate -> tube formation - neural crests will lose contact and migrate to the developing embryo -Neural plate thickens folds -Narrow band of cells between the 2 cell types epithelium to mesenchymal transitional lose connection from neighboring cells become mesenchyme -Neural crest cells have spontaneous ability to move above from epidermis and go from epithelium to mesenchymal transition * Can migrate quite a distance -Migratory behavior is associated with changes in cell adhesion properties. -To migrate neural crest cells will undergo a process known as -epithelial-to-mesenchymal transition (EMT).NEURAL CRESTstem cell like population, give rise to a broad array of derivativesNeural crests providesprovides innervation to the entire digestive systemCranial neural crest(derived from the hindbrain) migrate dorsolaterally and contribute to the craniofacial mesenchyme that differentiates into cartilage, bone, cranial ganglia (neurons and glia) and connective tissues of the facePharyngeal archesorigin of craniofacial skeletal elements derived from the neural crestCardiac neural crestcan give rise to the entire musculo-connective tissue of the large arteries as they arise from the heart and to the septum which separates the pulmonary artery from the aorta. -septum of the outflow tract of the heart & wall of large arteries -first somite to fourth somiteVagal neural crest-Parasympathetic enteric ganglia of the gut -First somite to seventh somiteTrunk neural crest-Melanocytes, dorsal root ganglia, sympathetic ganglia & adrenal medullaSacral neural crest-parasympathetic enteric ganglia of the gut -the most distal portion of the neural crestDEFECTS OF NEURAL CRESTdoesn't migrate to proper location/doesn't differentiate correctlyNeurocristopathies-Group of diseases associated with abnormal development of the neural crest. -Result of defects in neural crest cells themselves but also of defects in the environment through which they migrate. -Defects affect only a single derivative of the neural crest, whereas other defects result in a wide array clinical manifestations.Hirschprung's Disease-Rare congenital disease 1:5000 live births -Mutations in Sox10 and Endothelin Receptor B -Aganglionic megacolon (absence of enteric neurons in the colon) -Often associated with pigmentation defects and deafnessTreacher Collins Syndrome / Mandibulofacial Dysostosis-Autosomal dominant craniofacial disorder (1:50,000 live birth) -Mutations in the TCOF1 gene, which encodes the nucleolar protein Treacle1 -Minimum number of cell death --> excessive cell death (deficiencies in number of neural crest present in early embryo)Madibulofacial dysostosis Diagnosis1st and 2nd branchial arch syndrome (Treacher Collins Syndrome) Clinical diagnosis: - Hypoplasia of facial bones (mandibule and zygomatic complex) - Downward slanting of palpebral fissures - Defective middle ear ossicles (hearing loss) - Alterations of outer ear shape and position - Dental malocclusion - Abnormal spacing and reduced number of teeth25 days-Pharyngeal pouches to which the neural crest cells will migrate28 daysEctoderm contribute to sense organsSense Organs• The sensory organs (epithelium of the nose, lens of the eye and inner ear) originate from thickening of the ectoderm in the head region, known as cranial placodes.cranial placodes> are induced by surrounding tissues > are thickenings of the cephalic embryonic ectoderm (thickened ectoderm at the anterior end of the embryo) Contribute to: + PITUITARY GLAND!!! / ADENOHYPOPHYSEAL GLAND + Cranial gangliaAdenohypophysis- anterior lobe of the pituitary gland - thickening of stomodeum (roof of mouth) - oral ectoderm invaginates to form RATHKE's pouch to form *ADENOHYPOPHYSES* - while the floor of the diencephalon invaginates to form the INFUNDIBULUM to form the "NEUROHYPOPHYSIS"Lens placodegive rise to lens (vision) >Diencephalon--> come in contact with ectoderm--> Induce thickening of ectoderm to give rise of to lens (optic cup give rise to retina)Otic placodegive rise to inner ear (hearing and balance) >Hindbrain region thicken --> invaginate to form otic pit --> put will eventually segregate to form otic vesicle --> semicircular canal (all components of inner ear)otic epitheliainduce chondrogenesis in the surrounding mesenchyme providing a protective and structural framework to inner ear.Olfactory placode- epithelium of nose (smell) - is required for normal forebrain development.Reciprocal interactions:-The lens is essential for the normal development of the adjacent structures, the retina, iris and overlying cornea. *Tissues neutrally induced will signal back to tissues inducing them --> determine their fate *required for normal brain developmentDelaminationSplitting or migration of one sheet into two sheets a. Trigeminal (ganglion CV V > ophthalmic : ophthalmic lobe of trigeminal > maxilomandibular: maxilomandibular lobe of trigeminal b. Epibranchial > geniculate: (dital ganglion CN VII > petrosal: distal ganglion CN IX > nodose: distal ganglion CN Xinvaginationthe folding in of a membrane or layer of tissue so that an outer surface becomes an inner surface > adenohypophyseal > lens > otic > olfactory