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last one Flashcards

1
Q

what is the leading cause of death worldwide

how many people have congenital heart diseases

A

cardiovascular disease

1%

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2
Q

which animals have a four chambered heart

which has a three chambered heart

what is the zebrafish heart like

and drosophila

A

humans, mice, chicks. only group to have a septum

xenopus- two atria and one ventricle. they still have their pulmonary and systemic circulation separated.

two chambered, one atrium and one ventricle and one circulatory system.

drosophila have a tubular heart, a single tube lined with valves that promotes the flow of blood in one direction.

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3
Q

human heart development:
what tissue is it derived from and what structure will be formed first and when?
how does the rest of the heart develop?

A

derived from the cardiogenic mesoderm which will form the cardiac crescent 2 weeks after fertilisation.

the cells in the crescent will migrate towards the midline and coalesce to form a single tube at around three weeks.
the tube undergoes assymetric cardiac looping which takes a week and will be complete four weeks after fertilisation.
then there is heart maturation, formation of the septa and valves. the heart will then be complete seven weeks after fertilisation.

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4
Q

how long does it take for the mouse heart to be completed

how does the zebrafish heart form

A

13 days. the crescent starts to form at 13.5 days. it is the same process as humans.

a cardiac disc forms at 20 hours, this is formed by the two groups of cells migrating to the midline
the disc extends to form the cardiac tube at 24 hours.
this will then undergo cardiac looping which is complete by 48 hours.

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5
Q

what are the common steps in heart development of all organisms

A

cardiac precursor cells are found as bilateral populations of cells around the midline.
this migrates to the midline and fuses to form a tube, the tube undergoes assymetric heart looping.
then the heart matures and forms the structures required for heart functioning.

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6
Q

what are the two origins of cardiac cells and what does each of them become
how are they laid out in the heart tube

A

the two heart fields.
the first heart field becomes the left ventricle and both atria. the second heart field becomes the right ventricle, both atria and the outflow tract.

the tube will be composed of first heart field cells, the second heart field cells are gradually encorperated into the heart as it undergoes morphogenesis.

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7
Q

what morphogen signalling is the cardiac mesoderm subjected to

what genes are expressed in each heart field

what do the cells do once they are specified

A

non canonical wnt which will promote specification into first heart field or second heart field progenitor cells.
they will then recieve either BMP or beta catenin FGF which decides whether they are first or second heart field.
nkx2.5 is expressed in both fields.
tbx5 is only in the first field.
isl1 is only in the second field.

once they are specified they migrate anteriorly to form the heart tube if they are the first field and the surrounding mesoderm if they are the second field.

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8
Q

how is chamber myocardium specified differently to myocardium that will not be in the chambers

how is AVC cell fate induced

A

notch tbx20 is important for specifying chamber myocardium, it will cause expression of Nppa and Nppb.

the atrioventricular canal is non chamber myocardium and it is specified by BMP2 which will cause tbx2 expression and this causes AVC cell fate.

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9
Q

what happens if you dont have tbx2

what if you dont have tbx20

A

the mice will have a widened AV canal and there will be increased expression of nppa (the chamber gene) in the AV canal.

mice will lose nppa expression and so will have no chamber identity, there will also be an expansion of tbx2 expression (avc gene) where the chambers should be.

tbx20 expression in the chamber myocardium allows chamber identity and represses tbx2 which causes AVC cell fate.

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10
Q

what animal is used to study heart looping

what are the basics of what happens

A

zebrafish

the cells in the heart tube grow in size and change shape, this varies depending on where in the heart the cells are.
the cells on the inner curvature of the ventricle will stay cuboidal, but cells on the outer curvature will grow more and elongate.
the second heart field cells add in as this happens.
there are assymetric cell movements at the poles of the heart.
there are regional changes in ECM composition, there will be more where the valves will form to make it stiffer.

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11
Q

how do the second heart field cells add into the heart

what happens to mice with no islet1

what does the addition of the second heart cells help to promote

A

they move posteriorly and add onto the bottom of the tube during looping.

they have a smaller heart that is incompletely looped.

looping

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12
Q

what do individuals with heterotaxia also normally have

what is situs invertus and how many people have it

what is situs ambiguous

A

congenital heart defects.

1 in 10,000 have a complete reversal of organ organisation with no symptoms.

a loss of concordance of organ laterality , not a full reversal only some.

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13
Q

where is nodal expressed before organ formation and what does loss of this nodal cause

what is the homologue in drosophila

A

it is assymetrically expressed in the left lateral plate mesoderm.
loss of nodal results in disrupted organ assymetry

spaw

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14
Q

what is the cupfers vesicle and what does it allow to happen

A

it is a transient cup shaped organ at the posterior of the embryo.
it is lined with motile cillia which beat in a clockwise movement and this creates directional fluid flow in the cup.
causing higher levels of ca on the left side of the cup and this causes the expression of nodal on the left lateral plate mesoderm.
nodal will turn on genes in the left half of the cardiac disc, cyclops and lefty2.
this allows correct looping

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15
Q

what happens if there is loss of assymetric nodal expression

what happens to humans with mutations in cilliary genes

A

there is randomisation of lateralised gene expression and then randomisation of directional heart displacement and looping.

heterotaxia and congenital heart defects.

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16
Q

what is the heart doing at the same time as it is developing and why

A

pumping.
this is because blood flow is important for gene expression of flow responsive genes. different levels of flow and stretch will activate various genes.

the form affects the flow, and then the flow affects the form.

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17
Q

Roux experiment

A

at the two cell stage of development he killed one of the cells using a hot needle.
this resulted in a half embryo.

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18
Q

who came up with the cell theory and what was the theory

A

Cooke

he discovered cells by placing sections under a microscope.

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19
Q

Weissman theory

A

germ plasm determinants theory.
all germ cells have a set of determinants, somatic cells only have a subset of these which will determine that cells specific function and behaviour.

this was found to be not true, because the somatic cells have all determinants but they only express some of them.

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20
Q

hans driech experiment

A

allow a sea urchin to develop to the two cell stage and separate the two cells.
each cell was able to develop into a larvae.
this would have stopped their cell cell communciation and proves that normal development requires this.

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21
Q

what is ubiquitous

A

something very common in cells

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22
Q

paracrine

autocrine

juxtacrine

A

a cell secretes a ligand which binds to a receptor on a neighbouring cell.

a cell secretes a ligand which will bind to a receptor on the same cell.

the ligand is membrane bound and will bind to a membrane receptor on another cell and bring them into close contact.

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23
Q

why are mice a good/bad model to use

chicks

zebrafish

drosophila

A

good genetics, manipulatable, well established, expensive, slow breeding, ethical restrictions.

accessible embryology, low cost, ethical.

accessible embryology, reasonable cost, ethical

accessible embryology, well defined developmental stages, low cost, no ethical concerns, not a vertibrate.

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24
Q

how are flies kept in the lab and how do they breed

A

they are kept as livestocks at 25 or 18 degrees.
they are in tubes with food at the bottom and they lay their eggs on the food and the larvae eat the food.
the larvae then climb up the sides of the tube and become pupae and hatch into adults.
the whole life cycle lasts ten days.

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25
Q

what happen in the first three hours of drosophila development

what is formed after the first day

how does the larvea change from first to second instar

A

the egg has undergone gastrulation and being segmented and is now ready to develop.

the first instar larvae has formed and it is an eating machine and builds up many energy preserves.

they outgrow their skin.

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26
Q

how long after being an adult before flies mate

how long do they live

A

8/9 hours and they lay their eggs a day later.

they all live to 40 days and some can make it to 60.

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27
Q

Sturtevant 1913

1914 Bridges

1927 Muller

A

constructed the first genetic map and realised that genes are arranged in a linear order.

chromosomes contain genes.

X rays cause mutations and chromosomal rearrangements.

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28
Q

1979 Nusslein Wischaus

A

they did a saturation mutagenesis to identify genes involved in the development and patterning of the larval cuticle.
They established 26,000 lines and 18,000 of them were lethal mutations but hardly any affected larval patterning, most just killed the flies.
they created the field of developmental biology.

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29
Q

what chromosomes does the drosophila have

A

X, 2nd, 3rd, 4th, Y

30
Q

drosophila courting

A

it takes 10-15 minutes.
if you take a fly and raise it by itself and then introduce it to other flies it will know the mating routine, this means it is innate.
it involves singing, taste, vision and smell.

31
Q

spermatogenesis in drosophila

A

the tip of the testes has a group of cells called the hub which are surrounded by stem cells.
they will divide and the one closest to the hub stays a stem cell and the other one differenciates into a cyst and gives rise to sperm.
the hub cells secrete factors such as unpaired which maintains the stem cell fate.

32
Q

oogenesis in drosophila

why does the female only need to mate once

how is the egg laid

A

the female has ovaries which contain ovarioles which is where the egg develops
the ovarioles are on strings with stem cells at the tip

the seminal recepticle stores sperm, when the egg is on its way out it is fertilised and then drilled into a patch of food where it is laid.

33
Q

why is an ovariole like a timeline of a developing egg

A

the stem cells at the tip start to differenciate and form a cyst, one of the cells in here will form the egg and the others will be supporting cells that provide the egg with nutrients.
the egg moves away from the tip of the ovariole as it develops.

34
Q

what is the DNA like in the egg and the supporting nurse cells

A

the egg has a pronucleus.
the nurse cells have replicated DNA because they need to make lots of things to supply the egg with.
the nurse cells chromosomes are called giant/polytene chromosomes because they have duplicated but not separated.
some of them are fatter than others and have been separated and are replicating they are called puffs and are extremely active.

35
Q

what is cytoplasmic dumping

A

the cytoplasm of the nurse cells is packed full of gene products and mRNA.
this is moved into the developing egg via ring canals which are holes connecting the nurse cells and the egg.
as the egg grows the nurse cells shrink.
some of the factors entering the egg have a specific subcellular localisation due to the cytoskeleton.

36
Q

what happens when the egg is complete

what is under the shell

what happens to the nuclei when the egg is laid

A

a shell is put around it called the chorion.

the vitelline membrane which is hydrophobic and stops the egg drying out.

when the egg is laid the two pronuclei fuse to make a diploid organism.
then the nucleus divides 14 times without the egg dividing to create a syncytium where all the nuclei go to the periphery of the egg.

37
Q

how does the syncytium become many cells

A

membranes grow up from the outside and into the egg and divide one nucleus between each set of membranes to make each nucleus get pinched off into its own cell.

38
Q

what does the stat92E mutation do

A

removes segments A4 and 5.

39
Q

how many segments does the drosophila head have

A

three

40
Q

what is complementation testing trying to find out and what happens

A

they test to see if two mutations causing similar phenotypes are on the same of different genes.
they create a double mutant that contains both of the mutations.
if the double mutant shows a phenotype then the two mutations are on the same gene and they fail to complement eachother.
if there is no phenotype then the mutations are on different genes and do complement eachother.

41
Q

how do we know that nusslein and wischaus found saturation

A

they found 580 mutations causing embryonic phenotypes and 139 of these were complementation groups.
this means they hit the same 139 genes approx four times to get the 580 phenotypes
this means it is likely that they found all possible mutations and this is called saturation.

42
Q

what were the four main groups of phenotypes that nusslien and wischaus found

A

gap genes where the mutation will cause a gap, eg knirps which causes T2, T3, A1-7 to not develop and this creates a very short larvae with only a head, T1, A8 and tail.

pair rule genes are mutations that cause every other segment to not develop, eg paired only has T1, T3, A2 etc.

segment polarity genes affect the symmetry of the naked cuticle and denticle belt in each segment, eg gooseberry removes the naked cuticle so the whole of every segment is hairy denticle

maternal affect genes eg bicoid.

43
Q

what is the heirachy of genes that divides the egg up into segments

A

first maternal genes are expressed that create morphogen gradients in the egg, this will define where the gap genes are expressed.
and gap gene expression is required for pair rule gene expression.
and finally the segment polarity genes are expressed and do the finer details of the segments.

44
Q

where is bicoid normally expressed and what is the mutant like

what happens if you implant wild type anterior cytoplasm into the anterior mutant egg

what about into the middle of the mutant egg

A

bicoid is expressed in the anterior of the egg.
the mutant doesnt have the head skeleton and thoracic segments and has an overall loss of anterior structures.

there is partial rescue of normal development of anterior structures

this caused ectopic head structures to form in the middle of the egg and thoracic segments to form on either side.

45
Q

how does bicoid affect pair rule genes

bicoid mutant and over expression

A

without bicoid, the anterior of the egg has faulty pair rule gene expression
a normal larvae will have seven segments that contain bicoid, in a bicoid mutant there are only five segments which are arranged abnormally.

when you over express bicoid you still have the seven stripes but they are pushed to the posterior side, because the bicoid conc in the anterior would have been too high for stripe formation. so the stripes form further away at a lower conc.

46
Q

what is bicoid and what does it do

A

a TF, it has many binding sites, some are high affinity and some are low affinity.

47
Q

how does bicoid affect kruppel and what kind of gene is kruppel

what type of gene is giant and how is it expressed

what does giant and kruppel do

A

where the bicoid conc is just right (goldilocks zone) kruppel expression is turned on, this makes a stripe of kruppel expression down the egg.
kruppel is a gap gene.

giant is a pair rule gene and shows many stripes of expression down the egg.

they both repress the gene called eve.

48
Q

what is eve gene switched on by and what type of gene is eve

A

hunchback

pair rule gene

49
Q

which segments is engrailed turned on in

what about eve and fushi tarazu

A

every segment

every other segment

50
Q

what is the difference between a parasegment and a segment

A

parasegments were placed before we knew how the real segments were arranged
these two terms define half a segment out of phase from eachother.
the segments are where the physical indentations form in the embryo, the parasegments are where the gene expression boundaries are.

51
Q

what are two examples of segment polarity genes

what happens when they are mutated

A

wg and hh

wg mutant causes only the denticles to form
hh mutant does this too but is fatter.

52
Q

how are hh and wg connected

what happens to cells that receive wg

A

if either one is lost then neither are expressed because they are dependent on eachother
they maintain eachothers expression and refine the segment borders
wg is expressed in one cell and hh is expressed in the one next to it, each of the cells gets a signal from its neighbour.

cells that recieve wg are repressed from forming denticle and become naked cuticle.

53
Q

what do hox/homeotic genes do and what are they controlled by

what is the antennapedia mutation

A

they are TFs which provide who am i information to each segment
they all bind to the same DNA sequence
they are controlled by gap and pair rule genes

instead of antenna a fly will have legs on its head

54
Q

what is a long germ band insect vs a short germ band insect and examples of each

A

drosophila are long germ band insects, all 14 of their segments are defined at once.
they have a quick embryogenesis of 24 hours but it is very complicated and involves many genes.

beetles and centipedes are short germ band insects, their development starts only with the head and thoracic segments, they add abdominal segments sequentially, there is a lump at the end called the posterior disc which buds off segments and gets smaller as it goes.
this is a more ancient method and is more simple.

55
Q

what is an intermediate germ band insect

what is vertebrate development most similar to

which genes control the segmentation clock

A

the fruit beetle does some segments all at once and then some develop one after the other.

short germ band because somites give off the segments

notch and delta

56
Q

why is MyoD a master regulatory gene

A

giving MyoD to cells that were already differenciated caused rapid loss of their differenciation characteristics and were converted into myoblasts and went onto form myotubes.

this means that MyoD is sufficient in making a cell differenciate into skeletal muscle.

57
Q

what are the other members of the MyoD family

what are they and what do they do

A

Myf5, myogenin, MRF4

they are TFs and they bind to the ebox sequence CANNTG.

58
Q

how does the somite divide into its main sections

sclerotome and dermomyotome and then the others

A

the somites are a ball of epithelial multipotent cells.
in the ventral medial quarter of the somites an epithelial to mesenchymal transition will occur and these cells will become the sclerotome.
the remaining cells are the dermomyotome.
the cells at both ends of the dermomyotome become mesenchymal and travel to the area between the sclerotome and the dermomyotome.
these cells form two groups, the epaxial myotome is closer to the neural tube and the hypaxial myotome is more lateral.
the cells that remain in the dermomyotome become the dermis.
the syndetome is also found in the gap with the myotome.

59
Q

where do skeletal muscles originate from

and when do they become specified

A

dermomyotome

they become specified for muscle fate when they delaminate from the dermomyotome.

60
Q

what do skeletal muscle progenitors express and where are they found

A

pax3 in the myotome

61
Q

where is myf5 expressed

are all the members of the MyoD family expressed in the myotome

A

somites, limb bud, branchial arch, head muscles, myotome.

yes they are but at different time points.

62
Q

Myf5 KO

MyoD KO

what does this mean

A

the mice are viable and there is no obvious muscle defect at birth, but there is a delay in the myotome formation until MyoD begins to be expressed.

the mice are viable and there is no obvious muscle defect at birth, but an increase in the mfy5 expression compensates for the lack of MyoD.

this is called functional redundancy, if you remove one of either MyoD or myf5 then the other will take over its function.
a double KO shows a complete absence of skeletal muscles and no presence of myoblasts. one or the other is required to generate myoblasts.

63
Q

myogenin KO

A

mice die shortly after birth from a diaphragm defect, the mice have myoblasts but they dont have myotubes.
this means that myogenin is required for the differenciation of myoblasts into myotubes.

64
Q

what is MRF4 required for

A

converting stem cells to myoblasts

but also converting myotubes to myofibres.

65
Q

how are the signalling pathways different in the epaxial and hypaxial myotome

A

they both express pax3.
expaxial has wnts coming for the dorsal neural tube and low shh from the ventral neural tube, this causes myf5 expression and leads to myogenin and MRF4 expression.
hypaxial has wnts from the ectoderm and BMP4 repression from the lateral plate mesoderm, this causes MyoD expression and leads to myogenin and MRF4 expression.

66
Q

why is BMP4 inhibition necessary for the cells in the hypaxial myotome

A

the cells from this group that will go onto form the limb need to delay their differenciation while they migrate to the limb.

67
Q

how does limb myogenesis occur

A

the cells migrating off the end of the dermomyotome express pax3 which drives cmet expression.
this is the receptor for HGF (hepatocyte growth factor)
HGF is expressed in the limb mesenchyme and this acts as a chemoattractant so the cells migrate towards the limb.
the cells split into two groups, dorsal or ventral, when they reach the limb and then they proliferate and activate the expression of myf5 and MyoD.

68
Q

what happens in the naturally occuring mutant splotch mouse

A

loss of pax3 function.
they have normal MyoD expression in the somites but none in the limb.
this is because the cells have failed to migrate to the limb because there is no pax3 to make cmet and allow them to detect HGF.

69
Q

what are satellite cells and where are they found

are they needed for embryonic development

what are they activated by and what do they do

A

skeletal muscle stem cells are found outside the muscle fibre under the basal lamina.

no they are not they are dormant.

injury, denervation or exercise
they express the same genes in the same order as what happens in embryonic development of muscle.
but they always divide so that they maintain the stem cell pool.

70
Q

how many satellite cells are there in the adult and the embryo

what is caused by having too many satellite cells or too little

A

satellite cells represent 32% of of muscle cells in the embryo.
they are 5% of muscle cells in the adult.

not enough of them causes weak muscle regeneration and muscle dystophies, sarcopenia (loss of muscles in aging), and cachexia (loss of muscle because of cancer)

too many causes purturbed regeneration leading to cancer and hyperplasia.

Dev Neuro (7 decks)

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