, CHAPTER LIST
Part I: General Embryology
Chapter 1: Introduction to Molecular Regulation and Signaling
Chapter 2: Gametogenesis: Conversion of Germ Cells into Male and
Female Gametes
Chapter 3: First Week of Development: Ovulation to Implantation
Chapter 4: Second Week of Development: Bilaminar Germ Disc
Chapter 5: Third Week of Development: Trilaminar Germ Disc
Chapter 6: Third to Eight Weeks: The Embryonic Period
Chapter 7: The Gut Tube and the Body Cavities
Chapter 8: Third Month to Birth: The Fetus and Placenta
Chapter 9: Birth Defects and Prenatal Diagnosis
Part II: Systems-Based Embryology
Chapter 10: The Axial Skeleton
Chapter 11: Muscular System
Chapter 12: Limbs
Chapter 13: Cardiovascular System
Chapter 14: Respiratory System
Chapter 15: Digestive System
Chapter 16: Urogenital System
Chapter 17: Head and Neck
Chapter 18: Central Nervous System
Chapter 19: Ear
Chapter 20: Eye
Chapter 21: Integumentary System
,Chapter 1: Introduction to Molecular Regulation and Signaling —
Test Bank (20 Advanced MCQs)
1) Neural tube patterning failure
A newborn has severe midline facial anomalies and a single ventricle consistent
with holoprosencephaly. Genetic testing reveals impaired signaling required for
ventral forebrain and midline patterning. Which disrupted pathway best
explains this defect?
A. BMP
B. SHH
C. WNT
D. FGF
Answer: B
Rationale (very deep): Sonic hedgehog (SHH) is a key ventralizing morphogen
produced by the notochord and prechordal plate, instructing overlying neural
ectoderm to form ventral midline structures of the forebrain. When SHH
signaling is reduced, the developing forebrain fails to separate into two
hemispheres (holoprosencephaly) and midline facial structures do not form
normally. BMP primarily dorsalizes tissues; WNT is central to posterior/dorsal
patterning and axis formation; FGF commonly supports proliferation, limb
outgrowth, and induction but is not the primary ventral forebrain midline
determinant.
Key words: SHH, holoprosencephaly, ventral patterning, prechordal plate
2) Failure of dorsal neural tube differentiation
A mutation causes excessive SHH activity in the developing neural tube. Which
change is most likely in neural tube patterning?
A. Expansion of dorsal interneuron domains
B. Ventralization with expansion of motor neuron domains
,C. Failure of notochord formation
D. Loss of posterior body structures
Answer: B
Rationale (very deep): SHH acts as a concentration-dependent morphogen that
specifies ventral neural tube fates. High SHH induces floor plate and motor
neuron progenitors; lower levels specify ventral interneurons. Excess SHH
shifts fate toward ventral identities, expanding motor neuron regions at the
expense of dorsal structures. BMP/WNT from the roof plate oppose this by
dorsalizing. Notochord formation is upstream and not the direct effect here;
posterior truncation is more typical of major axis/primitive streak disruptions
rather than SHH hyperactivity.
Key words: SHH gradient, ventralization, motor neurons, morphogen dose
3) Clinical teratogen timing: limb + craniofacial
A pregnant patient takes a drug at a dose that inhibits BMP signaling during
weeks 4–6. The fetus later shows abnormal digit separation and craniofacial
malformations. Which mechanism best links BMP inhibition to these
anomalies?
A. Loss of apoptosis and impaired tissue sculpting
B. Increased somite segmentation
C. Excess neural crest migration
D. Premature placental maturation
Answer: A
Rationale (very deep): BMP signaling participates in patterning and
programmed cell death (apoptosis) in several embryonic contexts. In the limb,
apoptosis in the interdigital mesenchyme helps separate digits; impaired
BMPmediated apoptosis can lead to syndactyly or abnormal digit patterns.
BMPs also pattern craniofacial structures via neural crest differentiation and
tissue interactions; disrupting these during organogenesis (weeks 4–8) yields
structural malformations. Somite segmentation is governed by oscillatory
pathways (including NOTCH/WNT interplay), not BMP as the dominant driver;
excessive neural crest migration is not a typical BMP inhibition outcome;
placental maturation is not the relevant developmental mechanism.
Key words: BMP, apoptosis, digit separation, organogenesis window
,4) AER and limb outgrowth
A fetus has severe limb truncation affecting distal structures (missing forearm
and hand elements). A defect is found in signaling required to maintain the
apical ectodermal ridge (AER) and sustain limb bud outgrowth. Which factor is
most directly involved?
A. FGF
B. SHH
C. BMP
D. TGF-β (general)
Answer: A
Rationale (very deep): The AER secretes FGFs (especially FGF8) to maintain
the progress zone and promote proximodistal limb outgrowth. Loss of AER-FGF
signaling causes distal limb truncation because mesenchyme fails to proliferate
and remain undifferentiated long enough to generate distal structures. SHH is
the ZPA signal for anterior–posterior patterning (thumb-to-little finger); BMP
helps sculpt and regulate apoptosis; TGF-β family is broad but the specific,
canonical AER maintenance driver is FGF.
Key words: AER, FGF8, limb truncation, proximodistal outgrowth
5) Axis specification and WNT
An early embryo shows failure of posterior body formation with severe caudal
regression-like features. The defect is traced to impaired signaling required for
primitive streak maintenance and posteriorization. Which pathway is most
implicated?
A. WNT
B. SHH
C. BMP
D. Retinoic acid catabolism only
Answer: A
Rationale (very deep): WNT signaling is essential for primitive streak formation
and maintenance and for posterior body development. Reduced WNT activity
,leads to impaired mesoderm formation and posterior truncation. SHH is more
about midline/ventral patterning; BMP contributes to dorsal/ventral and
ectoderm/mesoderm decisions but is not the primary primitive streak
maintenance signal; retinoic acid levels do influence patterning, but the
question emphasizes primitive streak/posteriorization—classic WNT territory.
Key words: WNT, primitive streak, posteriorization, caudal truncation
6) Morphogen gradient interpretation
A mutation prevents cells from downregulating receptors after morphogen
exposure, causing them to “over-read” a gradient and adopt inappropriate
identities. Which concept best explains this?
A. Genomic imprinting
B. Threshold-dependent morphogen response
C. Meiotic nondisjunction D. X-inactivation skewing
Answer: B
Rationale (very deep): Morphogens (e.g., SHH, BMP) specify cell fate by
threshold effects—cells adopt different developmental programs depending on
the concentration and duration of exposure. If receptor downregulation fails,
signaling remains artificially high, causing cells to interpret the gradient as
“higher dose” than reality, shifting identities. Imprinting and X-inactivation are
epigenetic phenomena affecting allele expression; nondisjunction is
chromosomal segregation error.
Key words: morphogen gradient, threshold, receptor downregulation, fate
switching
7) Notch and segmentation
A fetus is found to have vertebral segmentation defects consistent with
abnormal somite boundary formation. A pathway known for “lateral inhibition”
and oscillatory signaling in somitogenesis is implicated. Which pathway is most
likely?
A. Notch
B. SHH
C. BMP
,D. VEGF
Answer: A
Rationale (very deep): NOTCH signaling supports segmentation clock
oscillations and boundary formation in somitogenesis. Disruptions lead to
segmentation defects of vertebrae and ribs. SHH patterns ventral neural tube
and somite derivatives (e.g., sclerotome induction) but segmentation timing is
classically Notch/WNT/FGF oscillatory interplay; BMP does dorsalization and
apoptosis roles; VEGF is angiogenesis.
Key words: Notch, segmentation clock, somitogenesis, vertebral anomalies
8) Ectoderm vs neural induction
An experiment exposes early ectoderm to high BMP levels. What fate is most
promoted?
A. Neural plate differentiation
B. Epidermal differentiation
C. Paraxial mesoderm formation
D. Endoderm specification
Answer: B
Rationale (very deep): BMP signaling promotes epidermal fate in ectoderm.
Neural induction requires BMP inhibition (via noggin, chordin, follistatin)
allowing ectoderm to become neural plate. Mesoderm and endoderm arise
primarily via gastrulation signaling networks including Nodal/FGF/WNT, not
BMP-high ectoderm default.
Key words: BMP high, epidermis, neural induction requires BMP inhibition
9) Midline defects and pathway localization
A mutation disrupts a transcription factor activated downstream of SHH in
ventral neural tube cells. Which phenotype best fits?
A. Dorsal spinal cord expansion
B. Ventral spinal cord motor neuron loss
C. Increased roof plate formation
,D. Failure of neural crest migration
Answer: B
Rationale (very deep): SHH activates ventral neural tube transcription factor
programs that specify floor plate and motor neuron progenitors. Disrupting
downstream transcriptional response means cells cannot execute ventral fate
even if SHH is present—leading to reduced/absent motor neuron domains.
Roof plate and dorsal expansion are associated with BMP/WNT dominance;
neural crest migration is a separate process influenced by multiple pathways
but not the most direct here.
Key words: SHH downstream transcription factors, motor neurons, ventral fate
10) Cross-talk: SHH and limb patterning
A patient has postaxial polydactyly. A defect is found in a pathway that
establishes anterior–posterior limb identity through a gradient in the limb bud.
Which signaling center and morphogen pairing is most correct?
A. AER—FGF
B. ZPA—SHH
C. Roof plate—BMP
D. Notochord—WNT
Answer: B
Rationale (very deep): The zone of polarizing activity (ZPA) secretes SHH to
pattern the limb along the anterior–posterior axis (thumb to little finger).
Altered SHH expression (ectopic, prolonged, or increased) can produce
polydactyly by expanding posterior identity programs. AER-FGF is
proximodistal outgrowth; roof plate BMP patterns dorsal neural tube;
notochord signals SHH (not WNT) for ventralization.
Key words: ZPA, SHH, polydactyly, anterior–posterior limb axis
11) Transcription factor role
A mutation disrupts a transcription factor that normally binds enhancer
regions to activate a cascade of organ-specific genes. Which best describes its
developmental role?
,A. Morphogen that diffuses across tissues
B. Master regulator controlling gene expression programs
C. Membrane receptor mediating juxtacrine signaling only
D. Enzyme for DNA replication during S phase
Answer: B
Rationale (very deep): Transcription factors are intracellular DNA-binding
proteins that integrate upstream signaling and activate/repress networks of
genes, often functioning as master regulators for lineage commitment.
Morphogens are typically secreted signaling molecules; juxtacrine signaling
(e.g., Notch) depends on cell-cell contact; DNA replication enzymes are not
specific developmental regulators of fate.
Key words: transcription factor, enhancer binding, gene regulatory network,
master regulator
12) Epigenetic dysregulation during development
A congenital syndrome involves widespread abnormal gene expression despite
normal DNA sequence. The defect is traced to failure of histone modification
patterns during early development. What is the most likely outcome at the
cellular level?
A. Random chromosomal nondisjunction
B. Inappropriate activation/silencing of developmental genes
C. Failure of ribosome assembly
D. Lack of fertilization
Answer: B
Rationale (very deep): Histone modifications control chromatin accessibility,
thereby regulating transcription. If epigenetic patterning fails, cells may
inappropriately turn on or silence genes required for positional identity and
differentiation, causing broad developmental defects. Nondisjunction is
meiotic/mitotic spindle error; ribosome assembly is not the primary link;
fertilization is upstream.
Key words: histone modification, chromatin, gene expression dysregulation,
epigenetics
, 13) Time-dependent teratogenesis
A teratogen inhibits FGF signaling during early organogenesis. Which defect is
most consistent with disrupted FGF roles during this window?
A. Distal limb truncation
B. Failure of neural tube closure from folate deficiency
C. Holoprosencephaly due to SHH loss
D. Hemangioma from VEGF excess
Answer: A
Rationale (very deep): FGF signaling is central to proliferation and outgrowth
in structures like limb buds (AER-FGF). Blocking it during weeks 4–8 can
produce limb truncations. NTDs are strongly linked to folate metabolism and
neurulation; holoprosencephaly aligns with SHH; hemangiomas relate more to
vascular growth regulation.
Key words: FGF inhibition, organogenesis timing, limb truncation, AER
14) Ligand-receptor specificity
A mutation prevents secretion of a signaling molecule, but receptor and
downstream intracellular machinery are intact. Which class of developmental
regulator is most likely affected?
A. Secreted morphogen
B. Nuclear transcription factor
C. Cytoskeletal motor protein
D. DNA repair enzyme
Answer: A
Rationale (very deep): Many patterning cues are secreted ligands
(morphogens) that must be exported to establish gradients (e.g., SHH, BMP,
WNT, FGF). If secretion fails, signaling cannot reach target tissues, despite
intact receptors and downstream effectors. Transcription factors act inside the
nucleus; cytoskeletal motors influence movement but not secreted signaling;
DNA repair is not primarily secretion-dependent.
Key words: secretion defect, morphogen, gradient failure, ligand
Part I: General Embryology
Chapter 1: Introduction to Molecular Regulation and Signaling
Chapter 2: Gametogenesis: Conversion of Germ Cells into Male and
Female Gametes
Chapter 3: First Week of Development: Ovulation to Implantation
Chapter 4: Second Week of Development: Bilaminar Germ Disc
Chapter 5: Third Week of Development: Trilaminar Germ Disc
Chapter 6: Third to Eight Weeks: The Embryonic Period
Chapter 7: The Gut Tube and the Body Cavities
Chapter 8: Third Month to Birth: The Fetus and Placenta
Chapter 9: Birth Defects and Prenatal Diagnosis
Part II: Systems-Based Embryology
Chapter 10: The Axial Skeleton
Chapter 11: Muscular System
Chapter 12: Limbs
Chapter 13: Cardiovascular System
Chapter 14: Respiratory System
Chapter 15: Digestive System
Chapter 16: Urogenital System
Chapter 17: Head and Neck
Chapter 18: Central Nervous System
Chapter 19: Ear
Chapter 20: Eye
Chapter 21: Integumentary System
,Chapter 1: Introduction to Molecular Regulation and Signaling —
Test Bank (20 Advanced MCQs)
1) Neural tube patterning failure
A newborn has severe midline facial anomalies and a single ventricle consistent
with holoprosencephaly. Genetic testing reveals impaired signaling required for
ventral forebrain and midline patterning. Which disrupted pathway best
explains this defect?
A. BMP
B. SHH
C. WNT
D. FGF
Answer: B
Rationale (very deep): Sonic hedgehog (SHH) is a key ventralizing morphogen
produced by the notochord and prechordal plate, instructing overlying neural
ectoderm to form ventral midline structures of the forebrain. When SHH
signaling is reduced, the developing forebrain fails to separate into two
hemispheres (holoprosencephaly) and midline facial structures do not form
normally. BMP primarily dorsalizes tissues; WNT is central to posterior/dorsal
patterning and axis formation; FGF commonly supports proliferation, limb
outgrowth, and induction but is not the primary ventral forebrain midline
determinant.
Key words: SHH, holoprosencephaly, ventral patterning, prechordal plate
2) Failure of dorsal neural tube differentiation
A mutation causes excessive SHH activity in the developing neural tube. Which
change is most likely in neural tube patterning?
A. Expansion of dorsal interneuron domains
B. Ventralization with expansion of motor neuron domains
,C. Failure of notochord formation
D. Loss of posterior body structures
Answer: B
Rationale (very deep): SHH acts as a concentration-dependent morphogen that
specifies ventral neural tube fates. High SHH induces floor plate and motor
neuron progenitors; lower levels specify ventral interneurons. Excess SHH
shifts fate toward ventral identities, expanding motor neuron regions at the
expense of dorsal structures. BMP/WNT from the roof plate oppose this by
dorsalizing. Notochord formation is upstream and not the direct effect here;
posterior truncation is more typical of major axis/primitive streak disruptions
rather than SHH hyperactivity.
Key words: SHH gradient, ventralization, motor neurons, morphogen dose
3) Clinical teratogen timing: limb + craniofacial
A pregnant patient takes a drug at a dose that inhibits BMP signaling during
weeks 4–6. The fetus later shows abnormal digit separation and craniofacial
malformations. Which mechanism best links BMP inhibition to these
anomalies?
A. Loss of apoptosis and impaired tissue sculpting
B. Increased somite segmentation
C. Excess neural crest migration
D. Premature placental maturation
Answer: A
Rationale (very deep): BMP signaling participates in patterning and
programmed cell death (apoptosis) in several embryonic contexts. In the limb,
apoptosis in the interdigital mesenchyme helps separate digits; impaired
BMPmediated apoptosis can lead to syndactyly or abnormal digit patterns.
BMPs also pattern craniofacial structures via neural crest differentiation and
tissue interactions; disrupting these during organogenesis (weeks 4–8) yields
structural malformations. Somite segmentation is governed by oscillatory
pathways (including NOTCH/WNT interplay), not BMP as the dominant driver;
excessive neural crest migration is not a typical BMP inhibition outcome;
placental maturation is not the relevant developmental mechanism.
Key words: BMP, apoptosis, digit separation, organogenesis window
,4) AER and limb outgrowth
A fetus has severe limb truncation affecting distal structures (missing forearm
and hand elements). A defect is found in signaling required to maintain the
apical ectodermal ridge (AER) and sustain limb bud outgrowth. Which factor is
most directly involved?
A. FGF
B. SHH
C. BMP
D. TGF-β (general)
Answer: A
Rationale (very deep): The AER secretes FGFs (especially FGF8) to maintain
the progress zone and promote proximodistal limb outgrowth. Loss of AER-FGF
signaling causes distal limb truncation because mesenchyme fails to proliferate
and remain undifferentiated long enough to generate distal structures. SHH is
the ZPA signal for anterior–posterior patterning (thumb-to-little finger); BMP
helps sculpt and regulate apoptosis; TGF-β family is broad but the specific,
canonical AER maintenance driver is FGF.
Key words: AER, FGF8, limb truncation, proximodistal outgrowth
5) Axis specification and WNT
An early embryo shows failure of posterior body formation with severe caudal
regression-like features. The defect is traced to impaired signaling required for
primitive streak maintenance and posteriorization. Which pathway is most
implicated?
A. WNT
B. SHH
C. BMP
D. Retinoic acid catabolism only
Answer: A
Rationale (very deep): WNT signaling is essential for primitive streak formation
and maintenance and for posterior body development. Reduced WNT activity
,leads to impaired mesoderm formation and posterior truncation. SHH is more
about midline/ventral patterning; BMP contributes to dorsal/ventral and
ectoderm/mesoderm decisions but is not the primary primitive streak
maintenance signal; retinoic acid levels do influence patterning, but the
question emphasizes primitive streak/posteriorization—classic WNT territory.
Key words: WNT, primitive streak, posteriorization, caudal truncation
6) Morphogen gradient interpretation
A mutation prevents cells from downregulating receptors after morphogen
exposure, causing them to “over-read” a gradient and adopt inappropriate
identities. Which concept best explains this?
A. Genomic imprinting
B. Threshold-dependent morphogen response
C. Meiotic nondisjunction D. X-inactivation skewing
Answer: B
Rationale (very deep): Morphogens (e.g., SHH, BMP) specify cell fate by
threshold effects—cells adopt different developmental programs depending on
the concentration and duration of exposure. If receptor downregulation fails,
signaling remains artificially high, causing cells to interpret the gradient as
“higher dose” than reality, shifting identities. Imprinting and X-inactivation are
epigenetic phenomena affecting allele expression; nondisjunction is
chromosomal segregation error.
Key words: morphogen gradient, threshold, receptor downregulation, fate
switching
7) Notch and segmentation
A fetus is found to have vertebral segmentation defects consistent with
abnormal somite boundary formation. A pathway known for “lateral inhibition”
and oscillatory signaling in somitogenesis is implicated. Which pathway is most
likely?
A. Notch
B. SHH
C. BMP
,D. VEGF
Answer: A
Rationale (very deep): NOTCH signaling supports segmentation clock
oscillations and boundary formation in somitogenesis. Disruptions lead to
segmentation defects of vertebrae and ribs. SHH patterns ventral neural tube
and somite derivatives (e.g., sclerotome induction) but segmentation timing is
classically Notch/WNT/FGF oscillatory interplay; BMP does dorsalization and
apoptosis roles; VEGF is angiogenesis.
Key words: Notch, segmentation clock, somitogenesis, vertebral anomalies
8) Ectoderm vs neural induction
An experiment exposes early ectoderm to high BMP levels. What fate is most
promoted?
A. Neural plate differentiation
B. Epidermal differentiation
C. Paraxial mesoderm formation
D. Endoderm specification
Answer: B
Rationale (very deep): BMP signaling promotes epidermal fate in ectoderm.
Neural induction requires BMP inhibition (via noggin, chordin, follistatin)
allowing ectoderm to become neural plate. Mesoderm and endoderm arise
primarily via gastrulation signaling networks including Nodal/FGF/WNT, not
BMP-high ectoderm default.
Key words: BMP high, epidermis, neural induction requires BMP inhibition
9) Midline defects and pathway localization
A mutation disrupts a transcription factor activated downstream of SHH in
ventral neural tube cells. Which phenotype best fits?
A. Dorsal spinal cord expansion
B. Ventral spinal cord motor neuron loss
C. Increased roof plate formation
,D. Failure of neural crest migration
Answer: B
Rationale (very deep): SHH activates ventral neural tube transcription factor
programs that specify floor plate and motor neuron progenitors. Disrupting
downstream transcriptional response means cells cannot execute ventral fate
even if SHH is present—leading to reduced/absent motor neuron domains.
Roof plate and dorsal expansion are associated with BMP/WNT dominance;
neural crest migration is a separate process influenced by multiple pathways
but not the most direct here.
Key words: SHH downstream transcription factors, motor neurons, ventral fate
10) Cross-talk: SHH and limb patterning
A patient has postaxial polydactyly. A defect is found in a pathway that
establishes anterior–posterior limb identity through a gradient in the limb bud.
Which signaling center and morphogen pairing is most correct?
A. AER—FGF
B. ZPA—SHH
C. Roof plate—BMP
D. Notochord—WNT
Answer: B
Rationale (very deep): The zone of polarizing activity (ZPA) secretes SHH to
pattern the limb along the anterior–posterior axis (thumb to little finger).
Altered SHH expression (ectopic, prolonged, or increased) can produce
polydactyly by expanding posterior identity programs. AER-FGF is
proximodistal outgrowth; roof plate BMP patterns dorsal neural tube;
notochord signals SHH (not WNT) for ventralization.
Key words: ZPA, SHH, polydactyly, anterior–posterior limb axis
11) Transcription factor role
A mutation disrupts a transcription factor that normally binds enhancer
regions to activate a cascade of organ-specific genes. Which best describes its
developmental role?
,A. Morphogen that diffuses across tissues
B. Master regulator controlling gene expression programs
C. Membrane receptor mediating juxtacrine signaling only
D. Enzyme for DNA replication during S phase
Answer: B
Rationale (very deep): Transcription factors are intracellular DNA-binding
proteins that integrate upstream signaling and activate/repress networks of
genes, often functioning as master regulators for lineage commitment.
Morphogens are typically secreted signaling molecules; juxtacrine signaling
(e.g., Notch) depends on cell-cell contact; DNA replication enzymes are not
specific developmental regulators of fate.
Key words: transcription factor, enhancer binding, gene regulatory network,
master regulator
12) Epigenetic dysregulation during development
A congenital syndrome involves widespread abnormal gene expression despite
normal DNA sequence. The defect is traced to failure of histone modification
patterns during early development. What is the most likely outcome at the
cellular level?
A. Random chromosomal nondisjunction
B. Inappropriate activation/silencing of developmental genes
C. Failure of ribosome assembly
D. Lack of fertilization
Answer: B
Rationale (very deep): Histone modifications control chromatin accessibility,
thereby regulating transcription. If epigenetic patterning fails, cells may
inappropriately turn on or silence genes required for positional identity and
differentiation, causing broad developmental defects. Nondisjunction is
meiotic/mitotic spindle error; ribosome assembly is not the primary link;
fertilization is upstream.
Key words: histone modification, chromatin, gene expression dysregulation,
epigenetics
, 13) Time-dependent teratogenesis
A teratogen inhibits FGF signaling during early organogenesis. Which defect is
most consistent with disrupted FGF roles during this window?
A. Distal limb truncation
B. Failure of neural tube closure from folate deficiency
C. Holoprosencephaly due to SHH loss
D. Hemangioma from VEGF excess
Answer: A
Rationale (very deep): FGF signaling is central to proliferation and outgrowth
in structures like limb buds (AER-FGF). Blocking it during weeks 4–8 can
produce limb truncations. NTDs are strongly linked to folate metabolism and
neurulation; holoprosencephaly aligns with SHH; hemangiomas relate more to
vascular growth regulation.
Key words: FGF inhibition, organogenesis timing, limb truncation, AER
14) Ligand-receptor specificity
A mutation prevents secretion of a signaling molecule, but receptor and
downstream intracellular machinery are intact. Which class of developmental
regulator is most likely affected?
A. Secreted morphogen
B. Nuclear transcription factor
C. Cytoskeletal motor protein
D. DNA repair enzyme
Answer: A
Rationale (very deep): Many patterning cues are secreted ligands
(morphogens) that must be exported to establish gradients (e.g., SHH, BMP,
WNT, FGF). If secretion fails, signaling cannot reach target tissues, despite
intact receptors and downstream effectors. Transcription factors act inside the
nucleus; cytoskeletal motors influence movement but not secreted signaling;
DNA repair is not primarily secretion-dependent.
Key words: secretion defect, morphogen, gradient failure, ligand
