MM Embryology 2 Flashcards by X x

separation between neural plate and epidermis

neural crest induction

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expressed Wnt and e-cadherin during induction

epidermis

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expresses BMP and n-cadherin during induction

neural plate

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what is required for neural plate induction, antagonizes ventral Shh

BMP

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what mediates epithelial-mesenchymal transformation and downregulates E-cadherin in neural plate for later migration

Slug/Snail

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Zic7, Msx1/2, Pax3, Cadherin 6B

border specifiers: prevent neural crest progenitors from becoming epidermis or neural tube

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FoxD3 and SoxE

neural crest specification and delamination

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at delamination, NC cells are still

multipotent and heterogenous

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allows migration via actin polymerizatoin

Rho B

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expressed in interactions between NC cells

Cadherin 7

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dorsolateral migrators (between epidermis and dermis) become

melanocytes

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ventrolateral migrators (through anterior sclerodome) become

dorsal root ganglia, sympathetic chain ganglia, schwann cells (PNS)

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NC cells express Eph receptor so that

ephrins can prevent them from entering posterior somites

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cranial NC become

mesectoderm (CT of head and neck)

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pharyngeal arch a NC differentiates in is determined by

Hox genes

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Post-otic NC become

sympathetic ganglion, enteric nervous system, adrenal medulla

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BMP7 (from aorta) makes NC become

sympathetic ganglion

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GGF makes NC become

schwann cells

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Endothelin + Wnt makes NC become

melanocytes

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enteric plexus is derived from

NC tissue

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NC cells headed to enteric express ____ and ride along ____ gradient

Ret, GDNF

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what is required to migrate past the cecum?

endothelins

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agangliosis (no ganglions, pseudoobstruction and dilation) caused by

Chagas disease (parasite)

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Ret/GDNF defect causes agangliosis in

Hirshprung’s disease

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defect in ET-3 endothelin receptor causes

Megacolon! (no plexus past cecum)

What signals ectoderm to form neural plate?

inhibition of BMP signals

neural tube forms by zips from

the middle

defects in neural tube closure cause posterior herniations called

spina bifida

Least severe SB, open vertebra

occulta

second least severe SB, meninges exposed

meningocele

second most severe SB, meninges and cord exposed

myelomeningocele

most severe SB, cord exposed

myeloschisis

anterior hernias in tube

cranial bifidum

second most severe CB, brain out

encephalocele

most severe CB, no telencephalon (anterior embryonic forebrain)

anencephaly

what tube region grows fastest?

forebrain

intrinsic factor in A/P hindbrain

Hox

extrinsic factor in patterning hindbrain

retinoic acid

dorsal structures in brain: signal

BMP/TGFbeta from roofplate

ventral structures in brain: signal

SSH from notocord and floorplate

ventral patterning defects in brain result in

Holoprosencephaly (forebrain does not divide)

defects in synapse formation and refinement

autism, rett syndrome, x-linked retardation

Long-range attractive for axon pathfinding

Netrins, DCC

Long-range repulsive for axon pathfinding

Slits, Robo

Short-range attractive for axon pathfinding

Laminin

Short-range repulsive for axon pathfinding

Eph-EphR, Sema-plexins

while crossing, midline ____ interacts with axonal ______ to prevent recrossing

Slit, Robo

merkels cartilage (malleus and incus), mastication muscles

Arch 1

typanic cavity, middle ear,

Pouch 1

eardrum

Groove 1

stapes, styloid process, stylohyoid ligament, part of body and lesser horn of hyoid, muscles of facial expression

Arch 2

palatine tonsil

Pouch 2

common carotid, greater horn of hyoid, stylopharyngeus

Arch 3

thymus, inferior parathyroids (migrates below pouch 4)

Pouch 3

aorta, right subclavian

Arch 4

superior parathyroid, ultimobranchial body (thyromedullary cells)

Pouch 4

ductus arteriosis

Arch 6

laryngeal cartilages, larygeal and most pharyngeal muscles

Arch 4-6

all PA nerve components are formed by

neuroectoderm cells

all PA muscle comes from

mesoderm

Pouch 1 is between

Arch 1 & 2

malformed external ear? Check for _____ defects.

Arch 1&2

external face develops

4-6 weeks

primary palate develops

5-7 weeks

secondary palate develops

6-8 weeks

completion of soft palate

8-12 weeks

mouth forms from disintegrated oropharyngeal membrane at

4 weeks

this, derived from ectoderm and NC mesenchyme, forms frontal nasal process

periprosencephalon

frontonasal process becomes

medial and lateral nasal processes

mandibular and maxillary process come from

pharyngeal arch 1

clefts fill in by differential mesenchyme proliferation (rare site of defect)

merging

Epithelium-covered surfaces contact, fuse, and break down (common site of defect)

fusion

the three sites of facial fusion

MNP and maxillary, LNP and MNP, palatal shelves at midline

oronasal membrane breaks down when to form choana?

6 weeks

what allows horizontalization of secondary palate in week 8?

increased production and hydration of FCM

placodes arise ____ to neural crest, between _____ and epidermis

lateral, neural plate

placodes arise from panplocodal ______

ectoderm

placodes give rise to

special sense organs, cranial ganglia of branchiomeric nerves in pharyngeal arches

Six1&2, Six 4&5, Eya, surrounding tissue, Pax genes

Tfs and influences on placode formation

lens and olfactory system come from which placodes?

V2, V3

lens forms by

invagination

otic and nasal placodes form by

invagination and delamination

in olfaction, placode also gives rise to

basal cells and support cells

optic nerve and retina are located

in the optic stalk and cup, from the forebrain

neural crest contributions to eye

choroid, sclera, cornea, pupillary membrane, chambers of eyes

utricle, semicircular canal for vestibular system come from

dorsal otic vesicle

saccule and cochlea come from

ventral otic vesicle

Statoacoustic ganglion on CNVIII comes from

delaminates otic vessicle cells.

faces, simian crease, mental retardation, heart disease

Trisomy 21 (Down)

short stature, webbed neck, swollen hands, gonadal dysgenesis

Missing X (Turners)

midline defects, CNS malformations, CHD, poor growth

Trisomy 13

clenched hands, rocker-bottom feet

Trisomy 18

FGFR3 defect

achondroplasia

PAX6 defect

aniridia

NEUROD1 defect

pancreatic agenesis

TTF1 defect

thyroid agenisis

NKX2.5 defect

congetial heart disease

ZIC3 defect

holoprosencephaly (forebrain does not divide)

doublecortin defect

lissencephaly (smooth brain)

IUGR, premature, neurocognitive

nicotine

long philtrum, small eyes, CHD, growth deficiencies, behavioral

fetal alcohol

yellow/brown teeth, decreased bone growth

tetracycline

IUGR microencephaly, mental retardation, distal phalangeal hypoplasia

hydantoin (anti-epileptic phenytoin)

cleft palate, craniofacial dysmorphism, neural tube defects

retinoic acid (first five weeks)

short limbs, ears, cardia problems, GU anomalies

thalidomide

cataracts, CHD, deafness

rubella (week 6)

IUGR, micromelia, blindness, cerebral calcification, heptosplenomegaly

CMV (most common viral)

when is ionizing radiation an issue?

10-18weeks, at high dose

amniotic bands, cysts, twins can cause

mechanical malformations

apoptosis in blastocyst

outer signal inner (BMPs), only saved if in contact with BM

BMP7 activates MSX which inhibits FGF

apoptosis in digits

activation of FGFR in digits

syndactyly (webbed digits)

apoptosis in heart

makes two chambers into four

zVAD

inhibits apoptosis in heart

both great arteries connect to right ventricle

double outlet right ventricle

lens is made translucent by

apoptosis!

fusion of palate requires

caspaces!

50% of postmitotic neurons die postnatally by

apoptosis!

cysteine proteases that cleave after asparate residues

caspaces!

cytochrome c in mitochondria is sequestered from _____, usually blocked from release by ____

Caspase 9, BCL2

BAK and BAX

apoptotic signals that poke holes in mitochondria to leak cytochrome c

APAF1 from cytochrome c

cleaves caspase 9 to activate

active caspase 9

cleaves caspase 3 which starts proteolysis