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Introduction to Developmental Biology: The Final
Terms in this set (242)
A transcription factor that is needed in order to develop the heart. Its loss entirely stops the heart from being formed in the fly. In mammals the loss of this is not as detrimental, but will still cause the heart to loop incorrectly and lead to separation defects
Cells that are needed to form the valves and septa of the four chambered heart
Jelly-like substance secreted by the myocardium
When existing vessels split apart and form new vessels
Support cells for the vessels, regulating their flow and stability
Made from the mesenchyme adjacent to the pharynx, they are corresponded to the gill arches of fish ancestors, and contribute to structures of the lower face and neck
Endoderm that is extraembryonic and is referred to as the hypoblast
Reduced number of air sacs, due to a molecular defect or restricted lung growth
Arches 1-3 are...
Arches 4-6 are...
TF that gives competence to the foregut, allowing it to become the liver, where it binds to an enhancer region of albumin after having its expression controlled by BMPs. It is also involved in the migration of the heart forming cells of the mesoderm, as well as the
Biliary epithelium cells (BEC/Cholangiocytes):
A cell fate of hepatoblasts that line the bile ducts in the liver (they express CK19)
The area of the intestine associated with cell differentiation
Enterocytes primary function:
Absorption in the gut
The pocket of endoderm epithelium that will become the liver
Bi-potential primordial liver cells
An area containing the bile duct, portal vein, and hepatic artery. It runs parallel to the liver
Secrete antimicrobial peptides
Large suture areas that are at the corners of the vault bones that allow the skull to distort during birth
TF that is involved in the dorsal-ventral patterning of the limb. It is induced by Wnt7A, and mutants of it have "dorsalization" of ventral limb tissue.
Area that forms the heart. It is split into two fields
The Primary heart field:
The region that forms from the cardiac progenitors using tissue from the primitive streak, and that migrate cranially. These will form the cranial crescent lateral plate mesoderm. It is the main, but not the only, source of cardiac cells
The Secondary Heart Field:
The cells that contribute to the outflow tract of the heart, the right ventricle, and part of the venous flow in the forming heart
The arc in the cranial lateral plate mesoderm that is made up of the cardiac progenitors from the primary heart field.
The contractile smooth muscle that secretes ECM and makes up the heart, specifically the heart muscle, and is responsible for depositing cardiac jelly around the endocardium and in the extracellular matrix
The tubes that are formed from the left and right wings of the heart
Failure of the 2 heart tubes from the primary heart fields to fuse. These tubes normally fuse to form the heart and Cardia Bifida occurs when these two tubes to not fuse
Structural and functional division of the heart into its four chambers, and includes both the formation of the septa, and the formation of the valves. Differential growth of the septal musculature drives the formation of the septa, where two waves of differentiation form the septum premium and the septum secundum, which fuse together to form the divisions of the septa (and also leave openings for blood to flow through before birth
Relevance of Cushions:
Formation of endocardial "cushions" from the endocardium and neural crest drives valve and septa formation (epithelial-mesenchymal, as well as epicardium cells are also involved)
Tetralogy of Fallot (in general):
A rare heart condition caused by 4 heart defects at birth. cyanotic, skin turns blue, baby not getting enough oxygen, 4 malformations co-occur: narrow pulmonary artery, ventricular septal defect, overriding aorta, and enlarged right ventricle
dorsal aorta and vena cava (in general):
The Aorta and vena cava are initially symmetric, but after they complete development in the pharyngeal arches they lose their symmetry, as one of the copies degrades and the other differentiates (into either the aorta or the vena cava)
The process of making blood cells (red and white) that occurs predominantly in the liver of the fetus and the bone marrow after birth.
Begins in the wall of the yolk sac, but quickly transitions to the liver using primitive hematopoietic cells. Later definitive hematopoietic stem cells from the area around the Aorta will colonize the liver again. These definitive hematopoietic stem cells will colonize the bone marrow and the bone marrow will become the dominant source of blood cells in the post birth human
hemangioblasts and/or "blood islands":
Cells capable of creating blood cells, and that are among the first to functionally differentiate in the embryo, specifically the hemangioblasts generate hematopoietic progenitors (that will colonize the liver and bone marrow) and endothelial precursor cells (that will proliferate the capillary vessel network in vasculogenesis). It is notable that the first blood cells arise in the blood islands (hemangioblasts) of the yolk sac before the embryo proper has developed the capability of making blood cells.
The creation of vessels via the budding and sprouting of preexisting vessels
the formation of new (de novo) blood vessels from the endothelial precursor cells (which themselves arise from the hemangioblasts)
The innermost germ layer in metazoans, termed the Definitive Endoderm, which is used to make specialized epithelial cells of the respiratory and digestive systems, and forms the thyroid, thymus, lungs, liver, biliary system, and pancreas. Definitive endoderm based tissues are important for exchange processes of gas exchange, digestion, nutrient absorption, metabolism, endocrine secretion, detoxification, and blood clotting
Diseases associated with dedicated endoderm:
Diabetes, cystic fibrosis, hepatitis, and colorectal cancer
Tissue that attaches the primitive gut to the posterior body wall, and is divided into the foregut, midgut, and hindgut based on the blood supply. It suspends the gut tube and allows the position of the gut tube to change during body folding. When organs fuse to the back of the body wall from being suspended in the body cavity, they become known as secondary retroperitoneal (ascending and descending colon, duodenum, and pancreas)
Thyroid, Esophagus, Lung, Liver, Biliary Tree, Stomach, Pancreas
Secreted by Type 2 alveolar cells. Function to reduce the surface tension of the thin liquid surface of the alveoli and allows for the alveoli (and by extension the lungs) to expand and fill with air
Loss of Surfactant protein B (via a frame shift mutation in SP-B) is...
typically fatal in newborns by 1 year
mucocilliary epithelium is composed of...
Multiciliated, Mucus Secreting, and Immune cells. All of these are patterned in the tissue by lateral inhibition, giving this tissue type its distinctive appearance. Notch is used for this form of patterning.
The organ develops in the body wall
Organs outside of the peritonin that fuse to the posterior body wall after having formed in the body cavity
Stays suspended in the body cavity, does not fuse to a body wall
pioneer transcription factor:
Are used to establish competency for later factors, and typically arrive in the tissue first
Bi-potential precursor cells that can make either hepatocytes (expressing albium) or biliary epithelial cells (expressing cytokeratin-19)
The division of the bones of the head:
the neurocranium and the viscerocranium
The bones that surround the brain and sensory organs
The bones that make up the face and pharyngeal arches
A condition where the sutures close prematurely, most often affecting sagittal and coronal sutures. This occurs when the progenitors cells of the osteoblasts in the in the nascent sutures differentiate too soon. This can be caused by teratogens, intrauterine restrictions, and the genes of Crouzon, Apert, FGFR2, FGFR3, and TWIST
Cyclopamine (and cyclopia):
One was a chemical found in Corn Lily that inhibits Shh. Because Shh is used for the patterning of the cranial midline, these defects caused the other term, a failure of the features of the face to move apart.
Frontonasal, Two Maxillary, Two Mandibular
The frontonasal facial prominence is made from...
neural crest from the forebrain and midbrain
The maxillary facial prominences are made from...
neural crest from the midbrain and hindbrain
The mandibular facial prominences are made from...
neural crest from the midbrain and hindbrain
Defects in the facial prominances cause...
cleft lip and cleft palate disorders.
Divisions of the sections of the limb:
stylopod, zeugopod, autopod
Most proximal division (like the Humorous)
Middle section of the limb (like the ulnar and radius)
Most distal section of the limb (like the hand and digits)
The Apical Ectodermal Ridge (AER) is an organizing center associated with...
Outgrowth of the limb (proximal-distal patterning of the limb bud). It is permissive (timing is irrelevant to its function) and is necessary and sufficient for limb outgrowth. FGFs are heavily expressed in this region (specifically FGF4 and FGF8, which the FGF both expresses and creates). These FGF TFs control the limb bud initiation.
The knockout of FGFs in the AER stops...
formation of the limbs (and also the lungs).
Describe the AER feedback loop that maintains outgrowth of the limb:
FGF10 activates Wnt, which in turn activates FGF8, which then activates FGF10 to continue the loop.
Possible mechanisms by which the AER functions to control limb growth:
Time Based: where the longer a cell has spent dividing, the more proximal fate it obtains, Expansion (French flag model): as cells are pushed out, they obtain a more distal fate, Intercalalary Specification: Division of limb fate by distal, proximal, and middle region by outgrowth.
zone of polarizing activity (ZPA):
The region specifies the specification of the anterior-posterior (cranial-caudal) axis of the limb.
Additional digits formed due to limb abnormalities
2 signaling regions at either end of the limb initially provide either a distal fate on the distal end) or a proximal fate (at the proximal end). As the limb becomes larger with outgrowth, the middle region of the limb is "freed" from the other signaling regions and obtains a "middle fate" outside of the influence of the other two signaling regions
Tissues that contribute to heart formation:
The mesoderm and endoderm initially, but are later joined by cells of the neural crest.
Describe the transcription factors associated with heart specification and the heart fields:
Wnt is initially pervasive in the mesoderm tissue, but is inhibited later in the anterior section of this mesoderm. Activin and TGF-B in the hypoblast and endoderm induce these tissues to become competent for heart formation (it will react to later signals from BMP2). Endodermal BMP2 activates Nkx2, which specifies the lateral plate mesoderm to become the heart. This is specification of the primary heart field.
In the secondary heart field, what genes and transcription factors are prominent:
Chord and Noggin are present, BMP and Wnt from the spinal cord mix to cause the formation of blood vessels and blood islands.
Irx4 is the TF for what process:
ventricular myosin (IE causes ventricles to form) and represses atrial myosin
Tbx5 is the TF for what process:
atria to form (atrialization)
Asymmetric gene expression established early in gastrulation determines...
The direction of cardiac looping and the eventual formation of the asymmetric heart.
How is cardiac looping signaled to occur:
By an unequal distribution of Nodal, where more nodal is expressed on the left side of the body (it is "pushed?" there by cilia.
The role of cell migration in heart tube morphogenesis/midline fusion:
As mesoderm cells migrate following internalization (from gastrulation), they establish a mediolateral and dorsoventral subdivision. This migration of mesoderm cells will form the primary heart field in the lateral plate mesoderm, and this tissue will be the primary tissue source for the forming heart.
The secondary heart field is involved in the formation of:
The outflow track, the right ventricle, and the venous flow in the forming heart.
Transcription factors for both the primary and secondary heart fields:
Activin and TGF-B (specifically TGF-1) are used to allow competence of the tissue, then BMP2 will specify the tissue into heart field).
Process by which Neural Crest Cells are involved in the formation of the secondary heart field:
Initially form in the brain, and migrates into the region, providing tissue and modulating the expression of FGF8.
Mef2 (and its associated family) is involved in...
Hand1 and Hand2 are involved in...
Formation of the left and right ventricles as well as the looping of the heart
Nodal invoved in cardiac looping though...
Concentration in the left lateral plate mesoderm, where it causes PITX2 expression, and torsion toward the left side for the heart tubes (there is no right side torsion, instead only left side torsion that loops the heart).
Holt Oram syndrome:
Mutations in Tbx5 cause numerous abnormalities with the formation of the chambers and heart tube, as well as atria septal and atrial conduction defects
The structural and functional division of the heart into its four chambers, and refers to the formation of both the hearts septa (its internal "walls") and the valves.
The two processes involved in Valvuloseptal morphogenesis:
Differential growth of septal musculature, and the formation of endochondral "cushions" from the endocardium (specifically by having these cells undergo epithelial-mesenchymal transition)
neural crest cells involvement in Valvuloseptal morphogenesis: Play a role in the development of the cushions
The Myocardium secretes ECM, after which endocardial cells undergo epithelial-mesenchymal transition and invade the ECM, then the septum and Valves are formed. It is of note that only the AV and OFT myocardium is competent to induce endocardial EMT
Valves formed during valvuloseptal morphogenesis are used to...
Stop the blood from being able to reverse intended direction in the heart.
When and where Primitive Hematopoietic stem cells are made:
Around day 17 (19?), and are derived from the yolk sac
When and where Definitive Hematopoietic stem cells are made:
Derived from the mesoderm around the aorta around day 27 (?)
Describe the Experiment that displayed the process of hematopoeitic stem cell migration:
A quail embryo was placed into a chicken yolk, and the blood was initially all chicken. By 5 days the blood was a mix of chicken and quail, and eventually all the blood was quail in origin. This demonstrates the hematopoietic stem cells colonizing the liver to allow blood to be made within the embryo itself
VegF is an early marker for...
Hemangioblasts, it is secreted from nearby mesenchymal cells to ac upon cells of the mesoderm where cells of the angioblasts and hemangioblasts possess receptors to regulate the formation of blood vessels.
VegF role in angiogenesis:
Induces tip and stalk cells to form (with a Notch differential signaling as the method to differentiate tip from stalk cells, with Notch and this transcription factor lower for the stalk cells (and the tip cells expressing Delta4), with the tip cell filopedia migrating and the stalk cells proliferating to allow extension (stalk cells also maintain the lumen of the vessel)
FGFR is the receptor for...
VEGF and it is located on the hemangioblasts and angioblasts
Mutations in VEGF1 cause...
Blood to form, but no blood vessels to form
Mutations in VEGF2 cause...
Neither blood nor blood vessels to form
Too much Hypoxia...
Decreases the secretion of VEGF, but at lower amount the need for oxygen will cause angiogenesis and the use of VEGF as an angiogenic factor
Nitric Oxide (NO) will cause...
Dilation of the blood vessels and will allow activation of proteases and the proliferation of endothelial cells (It will increase the proliferation of blood vessels)
VEGFR2 and Notch, and they have the cell surface molecule Ephrin-B2
VEGFR3 and have the cell surface molecule EphB4
Recall the themes of endoderm organogenesis:
Regionalizing via TF "codes", Activating TFs in a specific order to induce competence, induction, differentiation, and morphogenesis, Reciprocal mesenchymal-epithelial induction and transition of mesenchyme to epithelial tissue, Interaction with other tissues to differentiate
The two main process the lung undergoes:
Branching (16 times) and Maturation of epithelium and aveoli
Describe branching in lung development:
Typically done in the earlier stages of development, but also in the division of the bronchioles that occurs after the main rounds of branching. This process will occur 16 times.
Describe the maturation of the epithelium and alveoli process in lung development:
Occurs after the branching and continues after birth. This process is involved in the formation of specialized tissues in the lungs.
Specialized tissues of the lung:
multiciliated, secretory, neuroendocrine, and type 1 and type 2 alveolar cells
Secretory protein and contributes surfactant apoproteins A, B, and D, as well as proteases, antimicrobial peptides, cytokines, and chemokines
Many cilia that beat to remove mucus in the lungs
Mucus secreting and provide lubrication
Hypoxia and oxygen sensing cells, and signals to surrounding cells
Type 1 Alveolar Cells:
Majority (95%) and are responsible for gas exchange and fluid homeostasis and are not-mitotic
Type 2 Alveolar Cells:
Minority (5%), mitotic and secrete surfactant. They can become type 1 cells in repair
FGF for lung development is secreted from:
The cardiac mesoderm
FGF for lung development are used for:
The specification of lung progenitors. They are used to establish competency in the foregut endoderm
How lung, liver, and pancrease tissues are specified:
Depending on the dose of FGF Ligands in the foregut
FGF10 in the mesenchyme and mesoderm induces...
The budding of lung tissue and promotes cell proliferation and outmigration via chemotaxis (As does reciprocal signaling from Shh)
Branching proceeds towards...
A source of FGF, and FGF inhibitors are used later to limit further branching
BMPs for lung development are secreted by...
The septum transverse mesenchyme
BMPs used in lung development cause...
The endoderm tissue to become competent to the signaling of FGF. FGF is released from the cardiac mesoderm.
BMPs in the foregut endoderm regulate the expression of:
Without BMP to set up competency in the foregut endoderm, and without FGF to induce hepatic development, the foregut endoderm will become:
Noggin in the foregut endoderm inhibits:
BMP in the foregut endoderm inhibits:
The first sign of hepatic development is:
FoxA2 is a:
Pioneering Transcription Factor
Open up chromatin for interaction with hepatic factor BMP, and are needed for the competence of FGF and BMP (both hepatic factors)
main steps in liver bud morphogenesis:
epithelial changes, recruitment of endothelial cells
Liver cells begin liver formation by shifting from simple cuboidal epithelium to:
thickened pseudostratified epithelium, and forms the diverticulum
Transcription factor Hhex is used for:
Stratification, a relevant process for liver formation
TF Prox is used for:
Delamination, a relevant process for liver formation
Numerous waves of Wnt activation and inhibition are used during:
Hapatoblasts around hepatic portal vein are induced by the mesenchyme to increase CK-19 and downregulate Hepatocyte genes to become:
Biliary epithelial cells.
Hepatoblasts in the liver parenchyma differentiate into:
The liver matures by the secretion of:
Various TFs that control key liver genes to be expressed
Liver, if damaged, is capable of regenerating up to:
How is the liver capable of regenerating a large amount of its mass?
The proliferation of mature hepatocytes by the action of liver stem cells,
Process of liver regeneration is reduced by:
Cirrhosis and Hepatitis.
The default state of the foregut endoderm is: The formation of the pancreas, via Pdx1 being prevalent in the region.
The ventral pancreas requires what to form:
Pdx1 and low levels of Shh.
To stop the formation of ventral pancreatic structures forming on the dorsal side...
signals from the notochord repress Shh signals in the dorsal region.
Transription factors expressed in the dorsal pancreatic mesenchyme that are needed for dorsal pancreatic development: Pbx1 and Isl1
Isl1 is later used for the formation of:
Notch is also used to specify if the tissue of the pancreas will become:
endocrine (secretory) or exocrine (non secretory)
In the formation of the pancreas, initially how many buds form?
Dorsal pancreatic bud location:
Grows into the mesentery
Ventral pancreatic bud location:
Starts under the gall bladder.
Which pancreatic bud migrates during the fusion of the buds? The Ventral
Describe the process of pancreatic bud formation:
The Ventral bud will migrate to the dorsal side and fuse with the dorsal bud. Together these buds will then fuse to the dorsal body wall and become retroperitoneal.
Two ventral pancreatic buds form and migrate in opposite directions. This causes them to wrap the duodenum in attempting to fuse to the dorsal pancreatic bud. The duodenum will be blocked by this abnormal migration.
Duodenal Stenosis is caused by:
Errors in Shh signaling
Micro Lumen Fusion:
The pancreas forms a mass of clustered cells and then creates small lumens within the mass by apoptosis. These lumens are linked up until a branching shape is formed.
Seen in the lung and kidney, when directional cell growth of the epithelial cells causes them to proliferate outward with lumens already formed to make the branching structure.
Mechanism for B-cells replenishment:
They replenish themselves, they do not possess a dedicated stem cell population.
Relevance of pancreatic cells to stem cell therapies:
Cells that undergo differentiation to either an exocrine or endocrine fate can be converted back and forth through the use of transcription factors, meaning these cells can be used to replace lost exocrine and endocrine cells elsewhere.
Within the intestine, where Wnts are expressed to a very high degree?
In the crypt
Wnts expressed in the crypt are used for what process:
To drive the proliferation of the cells leaving the crypt. At the opposite end of the
The villus expressed what transcription factors?
TGF-B and BMP
TGF-B and BMP expressed in the crypt are used for what process:
To drive maturation and differentiation of the cells that Wnt transcription factors in the crypt have proliferated.
Inactivation of APC causes what?
It is a negative Wnt regulator, so can give rise to colo-rectal cancers as the Wnts produce cells in an uncontrolled fashion.
Ephs is expressed to a high degree:
In the crypt
Ephrins is expressed to a high degree:
In the Villus
Eph/Ephrin gradient in the intestines form:
The crypt-villus border.
Eph/Ephrin gradient is controlled by:
Eph/Ephrin gradient is responsible for:
Keeping the Planth cells (which have Ephs) in the crypt and away from the villus.
The temporomandibular joint was:
Evolved, ancestors did not possess one.
The bones of the pharyngeal arches were modified to form:
The larynx and middle ear
The chondrocranoum in ancestor fishes covered:
The chondrocranium's current function:
To cover the base of the brain, and now forms the occipital bones. Expansion of the brain caused this change.
The dermal bones expanded to form the:
The ancient chondrocranium was composed of three parts of paraxial cartilage elements:
The prechordal, The hypophyseal plate, and The parachordal. In humans, these bones fuse across the midline and form the ethmoid bone, which is the base of the sphenoid and occipital bones.
The modified vertebral element the occipital somites became the:
The majority of the cranial base ossified before birth via:
The membrane bone armor covered skull of ancestral bony fishes, and evolved later to form:
The flat membrane bones of the skull in humans (the calvaria) and many of the facial bones.
The anterior skull is formed form the:
The posterior skull is formed from:
The cranial vault bones are not completed by birth, why?
The soft sutures permit deformation in the birth canal to allow for birth.
The fontanelles are:
Larger suture regions at the corners of the vault bones. These ossify after birth.
Activating mutations in FGFRs contribute to the progression of:
In the formation of the skull, low FGF activity causes:
In the formation of the skull, high FGF activity causes:
TWIST and EFRINB1 are responsible for:
Neural crest cell sorting and FGFR inhibition.
Mutations in TWIST and EFRINB1 can result is the development of:
There are three sequential steps in development of the cranial midline:
Formation of the prechordal plate during gastrulation, Signaling from the prechordal plate to the forebrain, Signaling from the forebrain to the facial ectoderm
During the formation of the cranial midline, the level of Shh activity controls the:
Distance between the features of the face and the midline.
Very low Shh activity in cranial midline formation causes:
Very high Shh activity in cranial midline formation causes:
Disprosopus (duplication of some of the facial features across the midline)
Timing of Shh activity in cranial midline formation affects the:
Severity of the craniofacial defects
The most common defect in the forebrain of humans, where the brain hemispheres fail to form. This causes cyclopia and single nasal hole (olfactory primordia).
What causes Holoproencephaly:
An error in Shh signaling
Patterning of the facial primordia is controlled by:
The neural crests it is formed from
Transplanting the neural crest of one species into another causes:
The face to develop the donor specie's facial form. By making a duck-quail chimera, the form of the beak can be made to be a mix of the two.
High BMP expression in the maxillary and frontonasal processes of finches causes:
A larger beak to form.
Alterations in the amount of BMP activity in the frontonasal processes alters:
The shape of the beak.
The first pharyngeal arch is patterned by:
The DLX code, a method of controlling gene expression.
The first pharyngeal arch neural crest comes from the:
Fore and midbrain
The first pharyngeal arch does not express any:
HOX genes. There are HOX related genes for the first arch structure, these are the MSX, DLX, LHX, GSC (these are merely genes that have a relation to HOX genes, but are not actually HOX genes themselves), which are combined into different patterns to achieve different forms. Getting rid of one can cause the formation of a different pharyngeal arch.
A loss of the DLX 5 and 6 genes causes:
The mandible arch to become maxillary derivatives.
Clefting occurs when:
The prominances fail to fuse correctly, this fusion is mediated by the specialized median edge epithelium.
Cleft lip occurs when:
The maxillary and median nasal prominances fail to fuse
Cleft Palate occurs when:
The palatal shelves fail to fuse together in the pallet.
Proximal-Distal Limb Outgrowth is controlled by:
Anterior-Posterior Limb patterning is controlled by:
Dorsal-Ventral limb patterning is controlled by:
Wnt7A and LmxB1
The HOXd13 gene is required for the:
Apoptosis of the interdigital region
BMP is used between the "phalanges" to cause:
Apoptosis and free them of the surrounding tissue.
FGF8 is used in the region of the digits to control:
The number and length of the phalanges.
Noggin is expressed in the digits, because:
It inhibits BMP and stops the BMP from triggering apoptosis in an area where the phalanges are being formed.
2 signaling regions at either end of the limb initially provide either a distal fate on the distal end) or a proximal fate (at the proximal end). As the limb becomes larger with outgrowth, the middle region of the limb is "freed" from the other signaling regions and obtains a "middle fate" outside of the influence of the other two signaling regions.
The HOX genes clustes A and D are associated with:
The development of the outgrowth of limbs, specifically the 9-13 genes of both clusters.
HOXA13 and HOXD13 are used for the development of:
The digits, and can even replace one another; both must be knocked out to halt limb development. They are nested, as per the nature of HOX genes.
A disease where extra digits are formed and fused together due to an autosomal dominant defect in the HOXD13. A Hox protein misfolds as a gain of function mutation, and these misfolded proteins aggregate, causing irregular formation of the digits. Homozygous individuals for the disease individuals are more heavily affected.
ZPA uses what transcription factor as its "positional signal" to induce digit patterning?
As the cells of the presumptive hand are exposed to higher concentrations of Shh from the ZPA, they form:
More posterior digits. The expectation to this is digit 1, which is the most anterior digit; it is Shh independent, and will form even if Shh is knocked out.
Digit 2 relies on:
The concentration of Shh
Digit 3 relies on:
The concentration AND the timing of Shh expression
Digit 4 relies on:
The timing of the Shh expression
When Shh is knocked out in a limb, there is a loss in:
The formation of digits, and also a failure in the outgrowth of the limb. This may indicate that this transcription factor is important in regulating the growth of the limb, in addition to its importance for patterning the digits.
When the Shh repressor Gli3Xt is knocked out, what occurs?
The length of the limb is normal, but high levels of polydactyly are observed. Because GliXt isn't present to stop the expression of Shh, it is over-expressed and additional digits form.
A Shh enhancer that was found in the Ssq insertion site, and that increases the expression of Shh. It is also involved in the activation and repression of the Ets/Etv proteins, which control for either expanding or repressing Shh expression.
Deletion of ZRS positive controllers causes:
Reduced the control of Shh. The limbs to become truncated if this loss results in less Shh, or Polydactyl if this loss in control causes the loss of a repressor to Shh.
A condition when the distal segments of all 4 limbs fail to form due to a set of deletions in the LMBR1 gene.
In the Shh-FGF8 loop, Gremlin maintains the loop by:
inhibiting BMP (that would otherwise stop the loop from occurring) and inducing Shh to be expressed.
Wnt7a is important to the Shh-FGF8 loop, because it:
Induces and maintains the expression of Shh.
As the limb grows out, the ZPA descendants cannot express:
The loss of gremlin expression from ZPA descendants causes:
BMP to no longer be inhibited, so it can stop the loop, as well as the maintenance of the signaling sectors. This eventual cessation of the signaling centers stops the limb from growing any further
Wnt7A is expressed where?
In the dorsal ectoderm
Wnt7A is required to form:
The dorsal limbs (in the correct way)
Mutant Wnt7a limbs have:
A ventralized dorsal side (such as footpads on the opposite side of the foot).
Wnt7a induces and maintains:
Lmx1b expression in the limb mesenchyme
Knockout of Lmx1b causes:
Ventralized limbs to occur, as well as a lack of the patella to form.
Nail Patella Syndrome (NPS):
A disease caused by an autosomal dominant mutation of the Lmx1b gene that causes a loss of nails and the patella.
Limb identity (IE is the limb a forelimb of a hindlimb) is determined by:
Within the mesoderm, the PitX1 gene and the Tbx4 gene is expressed in the limb bud for:
The hindlimb to develop.
Tbx5 (also in the mesoderm, for the atria) is expressed in the limb buds of the:
The Tbx genes for limb formation ARE:
Necessary for correct formation of the limb (the loss of them causes the limb to not form),
The Tbx genes for limb formation ARE NOT:
Sufficient in inducing a forelimb or hindlimb fate.
Tbx4 placed in a forelimb bud that has a Tbx5 knockout can:
Rescue limb formation.
Placing Tbx4 and PitX1 in a Tbx5 knockout forelimb causes:
Partial conversion to hindlimb, as structures of the forelimb resemble structures associated with the hindlimb.
The knockout of PitX1 causes:
The loss of the hindlimbs, but the forelimbs will develop normally.
Loss of the hindlimbs due to defect/deletion of Pitx1 is notable because the loss of the hindlimbs is...
Asymmetric, with the right side hindlimb affected more than the left side hindlimb. Pitx2, a gene expressed only on the left side, may provide compensation and explain this phenomenon.
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