Fichas
Developmental Final
Fichas del conjunto (90)
- 1*List the 5 genes in order o Gene Hierarchy.
- 2*Explain loss of function experiment with Bicoid.If there was a Bicoid deficient mutant, The embryo would not develop a head. It would instead develop tail-> abdomen-> tail.
- 3*Explain the rescue process of a Bicoid mutated embryo. Explain what happens when Bicoid mRNA is injected in different parts of the embryo.For the embryo "rescue" experiment, he Bicoid mRNA was injected into the anterior part of the animal. The animal developed normally.
If the Bicoid was injected into the middle of the mutant, it would develop a head in the middle of the embryo (tail->thorax-> head->thorax->abdomen-> tail)
If the Bicoid was injected into the posterior of the wild-type embryo, it would create two heads!
- 4Give the 3 main steps in the mechanism of bicoid action. (*Explain how the Bicoid gradient forms.)1) Bicoid protein represses posterior determinants.
2) Posterior part of the embryo is regulated by the nanos and caudal genes.
3) Formation of the terminal ends f the embryo.
(1. Bicoid represses caudal translation in the anterior end by binding to the 3' UTR of caudal message
2. Bicoid activates the transcription of the hunchback gene which is set up in a gradient and is key in regulation of expression of the gap genes.) - 5Where in the egg is the highest concentrations of Caudal and Bicoid?Caudal Gradient: caudal is most prevalent in the posterior region and Bicoid is most prevalent in the anterior part of the egg.
- 6*What makes Nanos , where can it be found in the egg, and when is it translated? Mutations in Nanos also 'srew up what? What happens to Nonos that do not get transported?Nanos mRNA is made by the nurse cells and is transported to the posterior part of the egg by kinesin. Molecules involved in the transport bind to the 3' UTR of Nanos. Nanos is translated at fertilization.
Mutations that screw up Nanos also screw up pull plasm and no formation of the posterior part of the egg.
Nanos that are not transported become degraded or not made into protein. - 7What is the mechanism of Nanos Action?Represses the translation of hunchback. Hunchback is put in the egg by the mom and is repressed in the anterior end. Inhibition of translation of hunchback helps to reinforce the hunchback gradient and inhibits anterior formation. This results in different structures forming at the two ends.
- 8In what parts of the egg are the Acron and the Telson located?Acron is found in the tip of the head.
Telson is locatted in the tip of the tail. - 9*Explain the Torso gene.The torso gene is a maternal effect gene so the mRNA is made by mom and placed in the egg. *It is a membrane protein that is not localized because it is located everywhere. Torso RNA is translated and made into protein after fertilization. *It is a signaling molecule because it makes RTK (receptor tyrosine kinase).
- 10*What are the two possible outcomes for Torso mutants?1) Loss of function: Mom makes inactive torso mutant and the anterior and posterior tips are missing on the ends. The animals is all torso.
2) Gain of function: The mutant is always active. Receptor Tyrosine Kinase is only active in regions where the ligand binds to it. The animal is half head tip and halv tail tip. - 11*Explain the mechanism of torso.Because it is a RTK, there must be a ligand that binds to torso at the extreme ends. The follicle cells increase ligand to help the torso. The ligand is made by the torso-like gene. If not activated, it acts as though there is no RTK.
When toro-like gene binds to torso=> dimeriztion => autophosphorylation => cascade of signals => transcrition factor.
If bicoid is around the head tip is made (acron)
If no bicoid is present then the tail tip is made (telcan).
- 12Segmentation genes are ____ genes and are expressed via___.zygotic genes
gradient expressed - 13*What are the three classes of segmentation genes?1) Gap genes- setting up into broad region by the GAP genes which are activated or inhibited by the maternal effect genes
2) Pair-Rule genes: Dived body into para-segments that are not identical into adult segments. They act on the segment polarity genes.
3) Segment polarity genes: Responsible for the repeated structures within the segments (anterior and posterior specifically).
- 14What are the effects of a mutated GAP gene?Missing big pieces of the body.
Example: Hunchback mRNA (maternal and zygotic component) Hunchback is critical with in the gap genes because it regulates expression.
If there is a low level of hunchback gene transcription in the anterior of the embryo and inhibition of translation in the posterior by nano. Helps to set up hunchback gradient that by cycle 12 there is a steep gradient of hunchback in the middle of the embryo. - 15How does the hunchback gradient effect the Gap Genes?It stimulates the transcription of the anterior genes and inhibits the transcription of the posterior factors. Once activated by the maternal effect and the hunchback genes, other gap gene expressions are stabilized by interacting with one another.
*Once stimulated, hunchback inhibits 2nd neighbor genes. - 16How do GAP genes create sharp boundaries?Gap genes proteins can inhibit one another. This is done by the repression of transcription of other gap genes. They act at a distance on neighbors that are not connected to them.
- 17What do pair rule genes do? How many stripes? How many different pair rule genes are there?Pair rule genes divide the embryo into para-sagments and are expressed before individual cells form (cellularization).
The form 7 strips along the length of the animal (zebra stripes) occurs right before entering the MBT
Picture shows 8 differnt pari rule genes that are setting up parasegments around the animal before membrand form around the nuclei. GAP and pair rule genes are dividing the embryo before there are cells.
There are 8 different pair rule genes.
- 18Explain this in pair rule genes.Some pair rule genes express re, blue, red and blue, or neither. Each row of cells is a different set of pair rule genes expressed. There are different parts of each segment bein expressed in a particular cell.
- 19Explain the mechanism underlying Pair-rule gene expression.Pair rule genes are controlled by gap genes. Of the 8 different pairs of pair rule genes, there are 3 primary pair rule gens (such as hairy which is expressed first). The other5 pair rule genes are secondary (such as fushi terazu aka FTZ).
The primary pair rule genes interact with each other and regulate the secondary genes. The pair rule gene enhancers are recognized by gap gene proteins and there are different modules of these enhancers. The modules control information of a particular stripe. - 20How is Bicoid Gradient formed?1) Bicoid represses translation of the caudal gene by binding to the 3' UTR of caudal message. Bicoid represses caudal in anterior end.
2) Bicoid activates the transcription of the hunchback gene. The hunchback gene is set up in a gradien and is key in regulation of expression of the gap genes. - 21*Explain gap gene enhancers. *What happens if there is a mutation?They are gap gene proteins and they help in the formation of a particular stripe. There are different gap genes in different parts of the body.
If there is a mutation, then the strip is missing. If there is a mutation in a binder there is also a stripe missing. - 22How can stripe placement be altered?1) Mutation in enhancers
2) Mutation of gap gen that binds to that enhancer. - 23What are Segment polarity genes? When are they expressed? What are they involved in? How many stripes do they make?Segment Polarity Genes do not encode transcription factors but do code for signaling molecules to communicate with cells to tell formation.
Expressed after cells form (primary are before and secondary are after)
They are involved in cell to cell interaction and reinforce the segmental periodicy (they help to establish cell fates in each segments by what the pair rule genes are doing + cell to cell signaling).
They make 14 stripes along the embryo. - 24*Give an example of the segment polarity expression.Wingless gene and engrail: wingless is a part of the wnt family and sets up initial pattering in the embryo. It is expressed by different combination of pair rule genes and is anterior to cells expressing engrail. Wingless and engrail become neighbors and wingless is secreted and binds to the receptor of the engrail cells that cause an increase/synthesis of engrail.
- 25*Explain the mechanism of segment polarity in reference to engrail.Engrail is not a cell signaling molecule but is a transcription factor. Its transcription is stimulated by high levels of pair rule genes.
There are other combinations that repress its expression and it creates a distinct group of cells that are expressing engrail. - 26*What is engrailed? *Give an example.Engrailed stimulates the production of signaling molecules (such as hedgehog).
Hedgehog binds to patch and stimulates wingless. The 2 molecules next to each other (hedgehog and wingless) create 2 gradients that create stabilization due to their gradients and distinct boundaries between the 2 cell types which are sources of the gradient molecule.
- 27What can wingless and hedgehog gradient molecules do? How do we know?Wingless and hedgehog gradients specify cell fates along the segment.
Evidence is hound on the dorsal epidermis along the fly embryo where there are 4 different cell types that have different cell fates (3 make different hair types and 1 is bod or without a hair type). This can be changed by the expression of wingless or hedgehog patterning.
- 28*What do Homeotic Genes do? *What are the 2 groups of Homeotic genes present in flies and what do they do?Homeotic genes code for different structures of the animal such as legs, wings, and antenna.
The groups present in flies:
1) Antenna pedia complex made of 5 genes
2) Bithorax complex made of 3 genes. - 29*What is the homeotic Complex (Hom c)?Homeotic Complex (Hom C) is antenna pedia and bithorax together
- 30*What happens where there is a dominant mutation in the Antenna pedia? *What happens if ther is a recessive mutation in the antenna pedia?If there is a dominant mutant, then legs will grow out of the head in places where the antenna should be.
If there is a recessive mutant, antenna will grow out of the sockets were the legs should be in the second thoracic segment. - 31Explain gene mapping and the body plan to animals.The order of the homeotic genes along the chromosome reflects the expression along the body axis.
- 32*Where are most of the most 5' end expressed in the animal? *Where are most of the most 3' end expressed in the animal?Most 5' end is expressed in the anterior part of the animal.
Most 3' end is expressed int he posterior part of the animal. - 33How are homeotic genes regulated?Homeotic genes are initiated by the gap and pair rule genes and are expressed in the most posterior regions.
- 34*What was first look at genetically Antenna pedia or Bithorax? *What what the problem with this? *Results?When the technology became available, antenna pedia was first studied
It had a HUGE intro and this took a long time to look through.
Found homologous region found n other homolog genes. This regions is about 180bp (homeobox) and cods for protein (60aa). It makes the helix turn helix structure. It is a region found in a lot of genes and BINDS TO THE DNA. - 35What is the most important gene in the the set up of the dorsal gene? *What happens when this gene is made into protein? *What is the dorsal gradient a result of? What cells is it transported into the nucleus of?The most important gene in the set up of the dorsal gene is the maternal effect gene.
When made into a protein, it makes transcription factors (which is easily distributed).
Gradient of dorsal cell is a result of cell signaling. It occurs after the 14th cell division.
Only is transported into the nucleus of the ventral cells. - 36*What is a loss of function mutation in dorsal- ventral cell fates? *What is a gain of function mutation in the dorsal - ventral cell fates?Loss of function mutation results with no ventral part of the body. It is all dorsal.
A gain of function mutation results with the entire animal being ventralized. Instead of dorsal in only ventral cells, dorsal is transported to all the cells which in turn makes all of the cells ventral structures. - 37*Draw and explain the dorsal activation. *Explain the role of the Gurken/torpedo pathway and the spatzle/toll pathway.Because dorsal is everywhere in the embryo, there is no gradient and the signaling pathway to the nuclei relies on egg-follicle cell communication. The signals involved are in the gurken/torpedo pathwa and the asymmetric location of the nuleus is important.
Gurken is a signaling molecule made by the nucleus that doesn't diffuse very far away. Only the close follicle cells (highlighted in blue) get that signal and the torpedo is the receptor. The activated cells make up the dorsal follicle cells.
At MBT 13 spatzle/toll pathway activates. The Spatzle is located on the ventral follicle cells as a ligand. They secrete this and bind to the toll receptor on the embryotic cells.
- 38*What happens when toll is activated in the spatzle toll pathway?Toll acts on a complex called the Dorsal/Cactus complex when activated. Toll splits this complex so that dorsal is not bound to cactus and dorsal is able to move into the nuclei.
- 39*What is the effect of dorsal on cell fate when there is a) a lot amount of dorsal and b) an intermediate amount of dorsal?a) If there is a lot of dorsal, then mesoderm formation occurs.
b) If there is an intermediate amount of dorsal, then the nervous system and ventral skin is made. - 40*What are Deuterostomes? Give an example.Animals that when gastrulation occurs, the blastopore becomes the anus. The second opening (the deuterous) becomes the mouth.
Humans, Sea Urchins, and Amphibians are Deuterstomes. - 41*Draw and explain the early development of Sea Urchins.radial holoblastic cleavage
During blastula stage, 1 layer of cells
touches both the blastoceol and the hyalin.
- 42Explain the mechanism of blastula formation.1) Creation of cell glue through tight junctions.
2) The inn and outer surfaces are different from one another.
3) Cell division continues from blastula but the animal remains one cell thick.
4) Somewhere between the 9th and 10th cell division the species become different because the cells enter MBT. Here, cells extend cilia through the hyalin layer.
5) Cells spin around once the cilia form and rotate.
*6) Cells secrete hatching enzyme that dissolves the fertilization envelope and hatches. - 43*Why does the animal stay one cell thick even thought the blastula continues cell division?1) There is an increased pressure inside the blastocoel and that pressure is pushing the cells out and keeping them from the inside.
2) The cells are also attached to the hyaline layer. The cells grow procesis that grow out and attach to the hyaline layer. - 44Explain the Horstadius experiment in the establishment of the germ layers.In the experiment, animals were taken at the 8 cell stage and the embryos were divided in half.
Found that if a separated into single cells or divided vertically, each cell forms its own embryo.
If divided into a group of cells split horizontally, it would not create a complete embryo (either all animalized or vegitalized).
- 45Explain Horstadius's Experiment at the 64 cell stage.Took different layers of cell.
Animal layers:
animal1+ animal2 =2 ciliated balls of cells (animalized)
An1+An2+Vg1= incomplete- decrease in cilia
An1+An2+micromeres= Recognizable larva
- 46What are fillapodia? Draw and lable the first step in which they are used.Fillipodia are long cytoplasmic processes that move. They eventually migrate into the blastocoel via ingression. they are called the primary mechenchyme cells because they are the first mecenchyme cells that appear in the animal.
- 47Explain the mechanism for the first step in gastrulation. (change in shape of hollow cell ball)There is a decrease in the adhesion of the cells to the hyaline (about 2%) and huge decrease in adhesion to neighboring cells (about 2%). There is about a 100x increase to the basal lamina in the blastocoel. Adhesion molecules (glue) changes during this development.
- 48What is the molecular mechanism for the first step in gastrulation?1. There is a fibronectin-like molecule in the extra cellular matrix needed for the migration.
2. There is a sulfated proteoglycan molecule needed for the migration.
3. Paracrine factors Vascular Endothelial Growth Factor (VEGF) and Fibroblast Growth Factors (FGF) are secreted and attract the migrating cells. These attracted cells form around the site of secretion to form a ring around the equator of the embryo and start to form spicules. As these cell ingress and move out, the gaps left behind the migrating cells are filled by the neighboring cells. This makes the bottom flatten more then dimple making the archenteron.
- 49Explain the 3 phases of the Gastulation Process.1. Vegetal cells change shape and composition of the hyalline layer.Cells secrete that cause change in hyaline layer next to it. Part of these changes are Microfilaments (made of acting). Cells sink into blastoceol and hyalin differential expansion and buckles (invagination)
2. Archenteron elongates and cells change shape. They flatten, migrate and intercalate- This extends the archenterson.
3. Secondary mesenchyme forms at the tip of the archenteron. The filopodia extend and contact cells on the opposite side. When they contact them, they exert tension and pull archenteron to opposite wall of the embryo. Where it touches and eventually forms the mouth of the embryo.
- 50Explain the evidence that supports that when the filopodia extend and contact the target cells they exert tension and pull the archenteron to the opposite wall of the embryo. (There are 3)1. Can eliminate the secondary mesenchyme with a laser and the archenteron only gets 2/3 length to the other side.
2. there seems to be a specific target region of the secondary mesenchyme for the filopodia to contact.
3. If you prevent the filopodia from contacting the secondary mesenchyme, the filopodia will continue to move and the secondary mesenchyme breaks away and migrates to the target sites. - 51Walk though this diagram.Walk though this diagram.
- 52In amphibians, fertilization can occur where? What develops from where the sperm contacts the egg?Fertilization can occur anywhere in the animal hemisphere.
Where the sperm contacts the egg establishes the dorsal ventral polarity.(ventral- front is where sperm contacts egg) - 53Explain, in words of pictures, the rotation mechanism to form the gray crescent. (3 steps)1. The coritcal rotates about 30 degrees with the respect to the deep cytoplasm. The microtubule network is between the cortical and the deep cytoplasm.
2. the gray crescent is the region of the embryo where gastrulation starts. At fertilization, decision of where hthe blastopore forms at site of gastrulation and anus.
3. Sperm entry point is on the opposite side of the egg. This is where the mouth forms on the ventral side of the animal.
- 54What type of cleavage do amphibians have? Why?Amphibians have radial holoblastic cleavage.
This occurs because amphibians have more yolk than sea urchins and the cleavage plane slows when it reaches the yolk. When equatorial division occurs, it is unequal. (The larger cells in the vegetal pole are macromeres and the smaller cells in the animal pole are micromeres.) - 55How many cells are in a blastula? How is the blastocoel formed? What is the blastocoel's function?128 cells form a a blastula.
The blastocoel is formed by a sealing from the inside out done by the formation of tight junctions between the cells during division. This creates two compartments.
The function of the blastocoel is to prevent interaction between the animal and vegital cells.
- 56What triggers MBT? What does it cause? (3 causes)MBT is trigger by the ratio of cytoplasm to chromatin.
It causes:
1. An increase in transcription
2. Asynchronous divisions
3. The G phases are added back into the cell cycle. - 57What technique was used to study amphibian gastrulation? What was found?The technique used to study animal gasturlation was called vital dyes where they stained living cells to find out where the cells ended up.
Founded a fate map from this procedure. - 58Explain the Gastrulation fate map. What is found at the: a) vegetal pole (deep and superficial)? b) animal pole (before and after fertilization)? c) What is established after fertilization?a) At the deep vegital pole is mesoderm and at the superficial vegetal pole is endoderm.
b) animal pole is ectoderm before and after fertilization.
c) After fertilization the dorsal and ventral axis is established.
- 59Where does gasturlation start? Explain the cell movement in three steps during gastrulation.Gastrulation starts at the side of the embryo where the gray crescent formed.
1) Invagination occurs. There is a change in cell shape and bottle cells form. Bottle cells are essential for the initial invagination. Form at the sight of invagination.
2) Epiboly- the animal cells spread as a sheet towards the blastopore.
3) Involution- The cells get pushed inside and migrate along the surface of the inside of the cells. Cells just beneath the surface contact the basal region of the blastomeres. We know that the extra cellular matrix secreted by the blasomeres is essential because they support migration.
Fibronectin is important in the process for movement to occur.
- 60Explain an experiment to show that fibronectin is important during the movement process of gastrulation. What does fibronectin provide? Where do integrins that bind to fibronecting form?A short peptide was injected into the blastocoel that contained the fibronectin receptors that attached to the intigrin's RGD sequence. This was injected into the blastocoel and showed that cells that were trying to convolut went to grab on to the fibronectin but the molecules couldn't stick to anything and could not move on the surface. No involution into the blastocoel occurred. The cell moved but not into the inside. They piled up on the outside of the embryo and created a 'brainn-like' structure in the fact that there are folds on the embryo.
Fibronectin provides anchor and direction.
Appearing right before they are needed, integring appear on the surface of the mesodermal cells just before involution starts. - 61Explain the movement of cells on the lip of the bastopore.The first cells inside the blastopore are the bottle cells and they form the endoderm.
The second cells inside are the precordial plate cells that move i before the chordamesoderm. the chordamesoderm makes the notochord.
- 62Explain the movement of the ectoderm during gastrulation.Cells spread as a sheet toward the blastopore- epiboly. There is an increase of number of cells and cell division .
convergence->invention->intercalation (forms fewer layers of cells. - 63Explain the Hans Speman experiment to find the mechanism of gastrulation in amphpibian newts. (Experiment 1 Cleavage of Nuclei)Experiment 1found that cleavage of nuclei are identical and totipotent.
He took a new, single cell embryo and wrapped it with a tool with a piece of blonde hair and pulled so that the nucleus was only on one side of the embryo.
The nucleus began dividing only on one side of the cells. Eventually one nucleus crossed over. He tightened the loop during the 16 cell stage. Both parts of the embryo was able to make newts.
16 cell stage nuclei is still totipotent!!
- 64What was Spemont's second experiment and what were the results?Similar to the first experiment, but in the second experiment, Spemont lassoed the embryo at a right angle compared to the first. Only one embryo formed a normal embryo because it had the gray crescent while the other formed a ball of cells without the gray crescent.
Found that what mattered was which cells had the gray crescent. The one without the gray crescent had 3 unorganized germ layer and no notochord or nervous system. Thought the gray crescent was needed to initiate gastrulation and change cell fate. - 65How was determination found to occur in gastrulation?Spemond's first experiment showed that during early gastrulation, the cell fate is not committed and that during a short period of time, cell fates are established and cannot be changed.
He also transplanted future neuropath cells onto another animal in a place that would become the epidermis- results depended on when the experiment was performed. Early transplanted cells changed their fates while late transplnted cells formed a new neural plate. - 66*Explain the dorsal lip experiment done by Spemon and Mangold? What was the result?Took two colored newts and donated a dorsal lip to the host cell that already had a dorsal lip. Invagination occurred at the new site because the cells were already determined. The determined cells began making cortomesoder (notochord) and gastrulation occured like normal in both spots. 2 entire embryonic axes formed, resulting in the formation of siames twins. In looking at the transplanted dorsal lip, there appeared to be some of the donor cells but most were from the host showing induction and the formation of something it abnormal (ventral instead of dorsal structures).
Showed that only the cells in the dorsal lip had their fate determined at early stage of development.
- 67What did Spemont call the dorsal lip cells?Spemont called the dorsal lip the 'organizer' and because he thought that the induction occurred first, he also called it the primary induction (it's not)...
- 68What does the formation of the organizer depend on?The sequence of events for the formation of the organizer depends on the mesoderm between the animal and vegetal poles.
- 69*What did Nieuwkoop do and what did he find about the mesoderm? *What does the animal cap make? *What does the vegetal cap make? *How is mesoderm formed?Nieuwkoop chopped the poles in half and separated the animal and vegetal caps into separate cultures.
The animal cap makes the ectoderm.
The vegetal cap makes the endoderm.
Neither make mesoderm by themselves. It can only be made when the animal and vegetal caps are combined. - 70*What induces the dorsal mesoderm? *What makes the ventral mesoderm?Only in some of the endoderm cells can dorsal mesoderm be induced. These cells tend to be the cells directly underneath the gray crescent.
Endoderm beneath the sperm entry site make the ventral mesoderm. - 71*What Molecules are present in the Nieuwkoop Center responsible for the change during dorsal mesoderm induction? *What are their 2 types? *Where can they be found?Beta Catenins
They link the cytoplasmic region of cadherins to the cytoplasm(structural) and are also transcription factors that interact with the DNA in the nucleus.
During fertilization, BC move to the dorsal parts of the egg. - 72*What happens if Beta Catenin is removed form the egg?If Beta Catenin is removed from the egg via antisence by knocking down the presence of Betat Cadherins, there is no dorsal structure formation. (Loss of function)
- 73*What is an example of a gain of function experiment for Beta Catherin?Injection of protein or RNA (B-cat mRNA) into the ventral part of the egg would be a gain of function experiment. This would result in a second embryonic axis.
- 74What makes Beta cadherins? *What is the enzyme that is responsible for the phosphorylation and degradation of BC in the ventral part of the egg? How do we know this?BC is made from mom(maternal mRNA).
Glycogen synthase kinase 3 (GSK3) is responsible of degrading BC.
Know this from a gain of function experiment whereGSK3 was activated and spread everywhere which result in no BC and no axis formation. - 75*What is Beta catinin's job?BC is involved in movement along microtubules and where it stays, formation of dorsal mesoderm happens.
Beta catinin is a transcription factor which is a DNA bending protein.
Can activate expression of other transcription factors expressed in the Spamann orgainizer such as Siamois and twin. - 76*What is the organizer? *What are the characteristics of the organizer? (there are 4)The orgainizer is mesoderm which induces the nervous system to form the ectoderm above the organizer.
Characteristics:
1) Cells make dorsal mesoderm/notochord
2) Dorsalized surrounding mesoderm
3) Dorsalized ectoderm (nervous system)
4) Can initiate gastrulation movements. - 77*What do we know about neural induction? *How do we know that?Organizer makes molecules that are diffusable so that they can have an effect on other cells around them.
(Because the ectoderm becomes the nervous system, it is a paracrine factor. If dorsal lip is replaced with anectoder- no nervous system forms.)
We know this because one can have a filter that blocks cell processies but allows for the passing of molecules. - 78*What is the default mechanism of ectoderm cells?The default mechanism for ectorderm cells is nervous system.
- 79*What are Bone Morphogenetic Proteins (BMP4)? *What happens when BMP4s are not present? *What inhibits BMP4?BMP4s are made everywhere in the embryo. They act on ectodermal cells and cause the formation of skin.
Without BMP4, ectoderm cells form nervous system.
Organizer inhibits BMP4. - 80*What forms if: a) ectoderm is by itself? b)ectoderm+BMP4? c) ectoderm+BM4+ organizer?a) ectoderm is by itself-> Nervous system
b) ectoderm+BMP4-> skin
c) ectoderm+BM4+ organizer-> Nercous system - 81*Name 3 BMP inhibitors.Noggin, Chordin, Follistatin
- 82What can Noggin save? What happens if Noggin is injected into a wild-type embryo? What 2 things does Noggin secreted protein do? *Where is it located? *What is its mechanism?Noggin can save a fertilizedthat has been exposed to UV light so that there is no blastopore nor gastrulation. Noggin will form a blastopore and cause gasturlation.
If a normal embryo is injected with Noggin, the animal develops with all head.
Noggen secreated proteins:
1. Induce neural tissue
2. Dorsalize mesoderm cells.
Ngggin is located in the dorsal lip and later in the notochord.
Noggin's mechanism of action: Noggin binds directly to the BMP4s and this prevents Noggin from binding to receptors. - 83Where and when is Chordin formed? what can it cause? How does it work?Chordin mRNA is in the blastopore at the start of gastrulation.
Can cause the formation of a secondary axis (can induce twin in the animal) and in later stages forms the notochord (hence its name).
Binds directly to BMPs so that they cannot interact with their interceptors. - 84What stage in development was Follistatin discovered? What does it do? Where is it found?Follistatin was discovered in adults. It inhibits follicle stimulating hormones in the anterior pituitary. It also dorsalizes ectoderm which makes the nervous system (function of the organizer)
mRNa is in the dorsal lip and later in the notochord. - 85Our molecueles are _____ as in birds and mammals, and the site of these molecules are____. a) the same b) different c) similar These molecules are located where?a) the same
b) different
These molecules are located at the site of gastrulation. - 86a) Homolog of BMP4 is made by ______. b) Chordin homolog is made by the _____.a) decapentaplegic (DPP)
b) Short Gastrulation (SOG) - 87How were mammalian homologs founded? Does the order along the chromosome affect the order along the body axis?2 labs were next to each other. One was looking for the homologs of flies in the gens of the frog. Found similar genes with a 180 BP homeobox- almost identical. Since DNA makes RNA which makes protein, this coded for 60 similar amino acids between the speciesbecause the genetic code is degraded.
YES! - 88What are paralogs? What is the Hox code hypothesis?Chromosomal duplication
The pattern of Hox gene expression is something that specifies particular structures along the anterior/posterior axis along the animal.
- 89How was the Hox code hypothesis tested? What were 3 supports of this?Loss of function: Knock Out (KO) mice- test of Hox B4. If eliminated, the 2nd vertebrae axis that gets converted into the atlas would be disfunctional. Would not be able to twist head because it would have 2 atlases and no axis.
Supports:
1. Hox code is involved in patterning segments along the anterior/posterior axis of the body.
2. Members of a paralogs speciy for differnt organs in a small region of embryo.
Defects caused by KO genes are specific to the anterior region of expression. - 90How does Hox seem to be evolutionary?Hox cluster isn't present until animals.
All have regionalized expressionof homolog ubs expressed in the same region.
Zootype are similar for all animals (order of expression along the complex (anterior/posterior axis)
This is the way we know how to make wings, legs, and abdomen of specific animals is done by turning on specific parts of genes- instructional molecules are the same in all!
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- Fichas sobre Developmental Final, creado por McKenzie Pickett el 27/04/2015.
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