cells to organisms Flashcards

1
Q

What are the differences in pro and eukary genome organisation

A

Nucleus vs nucleoid

Nucleus (top) is a Eukaryotic compartment

Entrance and exit of material is tightly controlled

In prokaryotes nuclear material is arranged in the cytosol

introns spliced out in eukaryotes

Circular / linear

Histones / not

2 copies / 1 copy

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2
Q

binary fission vs mitosis/meiosis

A

Binary fission is simpler & quicker

A form of asexual reproduction.

Produces two identical daughter cells (like mitosis).

Some Eukaryotes do something similar

Meiosis in Euk – enables genetic novelty! Sex!

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3
Q

differences between rna polymerase in Eukary and Prokary

A

Complexity in gene regulation generated by transcription factors in Eukaryotes, rather than different σ factor subunits.

prokaryotic less complex

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4
Q

how did evolution of eukaryotes come about

A

Compartmentalisation
The evolution of separate compartments enables a broader set of biological processes to happen simultaneously

keeping biological processes that need to be sperate, separate

processes could be stopped if they happened in the cytosol

needs to be a concentration of factors in order for a reaction or process to happen

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5
Q

key features of eukaryotic nucleus

A

Entry and exit into the nucleus is tightly controlled via pores
Nuclear Lamina provides important anchor point for chromosomes

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6
Q

how does the nucleus import and export of materials

A

movement of biomolecules through the nuclear pore complex is tightly controlled

Nuclear pore complex contains many proteins

proteins and nucleic acids can only be transported in where and when they are needed to be

proteins require nuclear localisation (or import) sequence in order to be brought into the cell

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7
Q

how is the nuclear lamina arranged

A

chromosomes arent neatly arranged

heterochromatin located at the edge of the lamina whereas euchromatin is located more towards the centre

tethering proteins anchor chromosomes to lamina to maintain nuclear territories

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8
Q

how does mitochontrial fusion and fission work

A

Often touch or fuse other mitochondria & Exchange membrane

transfer genetic information

Can track this with flourescence

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9
Q

key features of endomembrane system

A

has a surface area 10x the size of the etermal surface of the cell

nucleus mitochondria chloroplasts

exchange of materials between parts of the endomembrane system through membrane bound vesicals

most proteins that have entered the system end up being secreted or at the cell membrane

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10
Q

how does the endoplasmic reticulum work

A

proteins are sorted depending on whether they are on free or membrane bound to ribosomes and the presence of signal sequencing

Proteins translated by free ribosomes will tend to require chaperone proteins to translocate them to target compartment

transport to golgi in a vesicle

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11
Q

how does the golgi work

A

The golgi is made up of a series of flattened stacks of membrane bound organelles called cisternae

Crucial for protein and lipid modification

Different cisternae may contain different enzymes or different reaction conditions

Sequential sugar modification is a good example of how the Golgi can work to separate process that need to happen separately

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12
Q

the roles of endosome system

A

store proteins so that they can be reused

can recycle and degrade membrane prtoeins from the cell surface

can be used to take in raw materials or nutrients

selectively transport materials to different places

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13
Q

why do cells need to communicate

A

homoeostasis and maintainance of internal state
buffers against changes in the external
environment
regulate development
cell cycle, cell movement, differenciation and
patterning

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14
Q

what is the flagellar synthesis constraint hypothesis

A

cells with flagella allow cells to be moved
the microtubule required for flagella formation is required to form spindle fibres in cell division
presence of both flagella cells and non flagella containing cells allow both movement and growth

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15
Q

what causes cell lineage

A

the turning on and off of genes as all cells have the same genetic material

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16
Q

what do cells require with multicellularity

A

Maintaining balance requires cell communication
requires the ability torecognise the same cells and different cells
cells need to be able to adhear to one another

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17
Q

types of cell response

A

cells may change gene expression
cells may move
contract
alter metabolism
proteins within may alter activity
concentration of ions may change

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18
Q

when is gene expression regulated

A

multipul levels
can be
regulated by RNA
messenger rna before translation
export from the nucleus
proteins can be regulated using post translational modifications

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19
Q

what is a cis-regulatory element

A

regions of DNA involved in gene regulation
provide the information for when when, how and at what levels genes should be expressed

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20
Q

what are trans-acting factors

A

they bind cis-regulatory elements. bind to regulate expression usually proteins. alter the activity

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21
Q

what do transcription factors do

A

transcription fo protein coding genes require the binding of RNA polymerase II
forms a complex that allows the start of transcription
(may bind indrectly to other proteins)
complex formed at the TATA box
diifferent transcription factors hve different specific sequences
unwind the DNA helix

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22
Q

what is the TATA box

A

region of DNA 30 base pairs up from the transcription start site that forms a section fo the promoter. Named due to the sequences of TATA DNA bases

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23
Q

What is different with specific transcription figures

A

They bind to regions of the enhancer or silencer regions
in enhancers activate transcription
in silencers bind repressor proteins that prevents transcription

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24
Q

what does specific transcription factors bind too

A

enhancer silencer
binding motifs (between 6-12)
short to increase probability of binding

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25
Q

how do specific transcription factors work

A

contain DNA binding domain (this being either an activation or repressor)
THis domains allows and encourages for interactions with other proteins

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26
Q

How do specific transcription factors influence the promoter

A

enhancer and silencer sequence are thousands of base pairs long when binded with STF can form a loop bringing it within the proximity of the promoter
interact with transcription initiationcomplex by the mediator complex

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27
Q

whats the effect ofenhancers and silencers on organisation of cells

A

as different cells have different specific transcription factors,different cells will activate different genes even though they have the same genome

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28
Q

Explain How Wnt works

A

The Wnt Pathway is critical for development of the embryo, and in tissue regeneration in adult bone marrow, skin and the intestines.
Wnt activates the Frizzled receptor on the cell membrane, the message is then carried through a series of steps to stop the degradation of β-catenin.activates Dishevelled. Dishevelled inhibits the β-Catenin Destruction Complex. Leading to the stabilization of β-Catenin which can then activate the transcription factor TCF.

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29
Q

Why do we need hypoxia sensing

A

detects when there’s a lack of O2 in tissues as O2 is less accessable this detection allows the stimulation of growth of blood vessels

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30
Q

main features of signaling

A

can diffuse over long distances
can create localised signals (only cells connected to cell recieve the signal
(achieve by membrane bound singal or
associated with extracellulr matrix)
transmited by a viety of mediums
(peptides, small molecules, metabolic products,
lipids)
receptors enable cells to react to signal
3D structure of receptor protein must be highly
specific for the binding of signaling molecule
typically found on the cell surface

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30
Q

what to do if you only have rna to applify

A

cDNA can be formed that is complementary to the mRNA showcasing the sequence free from introns

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31
Q

how do differences in hyprophobicity lead to different pathways

A

hydrophilic molecules wont dissolve in membrane therefore a receptor is likely found to combat this

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32
Q

type of signaling

A

contract/justacrine (direct contact), paracrine and autocrine secreted by extracellular space and endocrine signalling is produced locally and transfered through the organism through blood

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33
Q

protein phosphorylation is an example of what?

A

molecular switch that turns a pathway on or off

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34
Q

how are RTKs activated

A

dimerization and autophosphorylation this increases the activity of the recpetor enables the binding of adaptor proteins which are unable to bind without phosphorylated tyrosine

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35
Q

how are GTPases activated

A

are activated by the exchanging of GDP to GTP. they are off in GDP stage and on in GTP stage. They hydrolyse to terminate the signal

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36
Q

what does GDP require to be activated

A

requires a GEF (Guanine nucleotide exchange factor).

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37
Q

what is ras relationship with cancer

A

50% of human cancers have mutations in Ras. What those mutations do is lock Ras in the active form. What that means is once activated it cannot attenuate that signal and it is no longer transient therefore driving growth.

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38
Q

what are the three main domains of ras

A

p loop and switch 1 and switch 2

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39
Q

key mutations in ras

A

G12V, Q61N and S17N

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40
Q

what does S17N do

A

Unable to bind GTP

Still can bind GDP

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41
Q

what does Q61N do

A

Low rate of GTP Hydrolysis

Intrinsic GDP/GTP exchange ability

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42
Q

what a does G12V do

A

Low rate of GTP Hydrolysis

GAPs no longer increase GTPase Activity

43
Q

what do FGFs do

A

Regulation of cell growth and survival,

ii) regulation of cell differentiation, 

iii) regulation of embryonic development.
44
Q

how does FGF respond

A

its an RTK so can phosphorylate proteins within the cell FGF ligands form a complex with extracellular proteoglycans these allow them to bind to receptors
multipul layers of kinases allows for signal amplification can activate MEK
MEK can phosphorylate MAP Kinase molecules
MAP-kinase (Erk) translocates to the nucleus where it binds to and phosphorylates to modulate the activity of multiple transcription factors.

45
Q

how to proteins get to the correct location

A

specific petide motif or a single motif

46
Q

what is a stem cell

A

a cell that has the ability to self renew and differenciate

47
Q

how do the river anolgy and epigenetic landscape analogies differ

A

potency
in river cells are limited to particular tissues whereas in th eother cells make progressive choices about how to differenciate
developmental history
stem cell specification relies of differencial history but cells are able to respond to cues

48
Q

what are the types of potency

A

totipotent - all embryonic and extraembrionic tissues
pluripotent - can contribute to all germ layers
can poften produce all embryonic tissues but not extraembrionic tissue
multipotent- tissue or germ layer restricted
can generate multipul specialised cell types

49
Q

what type of stem cell are most embrionic cells

A

totipotent until morula stage

50
Q

what happens during the cleavage stage

A

rapid division, synchronous (all division occurs at the same time all in the same stage of the cell cycle), reduction division

51
Q

what happens in the blastula stage

A

division becomes asynchronus, fluid filled cavity forms (blastocoel), some specialisation forms

52
Q

what are the stages of development

A

cleavage stage, blastula, gastrulation,neurolation, tailbud

53
Q

what happens in gastrulation

A

the three germ layers separate endoderm, mesoderm and ectoderm. the blastula envaginates

54
Q

what happens in neurolation

A

ectoderms folds in on its self and merge together enclosing the neural plane.

55
Q

what is tailbud

A

phylotypic stage development of nortichord

56
Q

what did old models suggest about development

A

during the cleavage stage nuclear ‘determinants’ segregate to different cells. the uneven segregation leads to development of different cell fates. mosaic development results from autonomus specification of cells fate

57
Q

what suggested the old models of development were wrong

A

Half an embryo wasnt created in an experimental setting it was able to regulate and develop a full embryo with no missing parts. This suggested it was controlled via regulations

58
Q

what happened in the Spemann’s organiser experiment

A

dorsal lip of blastopore was transplanted into a host embryo on the opposite side. This new embryo was double headed with 2 connected complete embryo made entirely of the host cells not the donar cell. This suggested cell to cell signaling is important for regulating cell fate

59
Q

what is gene constancy

A

development does not involve a loss of genetic information rather the cells become different from one another during development through differential expression responding to cell signalling

60
Q

what proof is there of gene constancy

A

in cloned animals none of the gentetic material is lost the nucleus from a fully differenciated cell is used to generate clones. This then reprogrammes to be able to produece all types of cells

61
Q

how can signals be used as morphogens

A

diffusion from a source establishes a concentration gradient of secreted signal, cells sense the concentration and respond depending upon the signal therefore morphogen as ellicits different responces from cells depending on concentration

62
Q

what is the french flag model

A

signal source at one end of a bunch of cells
diffusion of signals establish gradient of morphogen,
the morphogen gradient allows cells to aquire information depending on their position to the source cells respond appropriately as a result of this

63
Q

what do the germ layers form

A

ectoderm - eperdermis and central nervous system,
mesoderm - notochord, dermis, skeleton, muscle, kidney heart and blood
endoderm - gut liver pancreas and lung

64
Q

whats the difference in formation at the equatorial region between early blastular phase and later

A

early only forms epidermis whereas later it only forms mesoderm cell. This occurs as the vegetal pole emits mesoderm inducing signal factors. This shows the mesoderm is derived from the animal pole

65
Q

whats different between dorsal and ventral cell in blastular phase

A

different types of cells are produced in different orientations. dorsal produces notochord and a little skeletal muscle cells whereas the vental side produces blood and smooth muscle

66
Q

What is the 3 signal model?

A

a model conveying the different patterning present within embryos. conveys there are 3 signals that induce differenciation.

67
Q

How is TGF beta cells present in development

A

they act as morphogens for formation, activin and nodal are present specifically

68
Q

what is the evidence that activin signals are required for mesoderm induction

A

a mutant receptor was formed without intracellular kinase domain when expressed in cells the activin receptor dimerises withnormal activin receptors and no signal can be transmitted no mesoderm is formed

69
Q

what are somites?

A

in vertebrates, all skeletal muscle is derived from somites. They are segmented blocks of mesoderm
new somites form from the anterior end of the presegmental plate mesoderm

70
Q

what are the derivatives of somites

A

scleratome forms in the ventral medial part of somite and differenciate as chondrocytes forming ribs and vertebrae
dermamyotone forms in the dorsal part and form the dorsal skin and deep muscle

71
Q

what are microorganisms

A

living organisms of microscopic size

72
Q

what are common features of pathogenic microbes that help them be good

A

Ability to enter the host and locate a suitable niche
Evade host immune responses both the innate and adaptive
Replicate within the host
Transmitted from infected to uninfected host

73
Q

common structural features of bacteria

A

pilus, capsule (can be there or not promotes sticking to surfaces and antiphagocytosis properties), cell wall, cytoplasm, plasma membrane, nucleoid, ribosomes and flagellum

74
Q

classifications of bacteria

A

based on shape
coccus: spherical
Coccobacillus: between coccus and bactillus
Bacillus: rod shape cylindrical
Vibrio: slightly curved long
Spirillum: wavy
Spirochetes: tighter coil spiral

75
Q

what are the differences between gram positive and gram negative bacteria

A

gram negative has an outer membrane whereras gram positive doesnt
gram positive has a thick peptidoglycan levelwhereas this is only thin in gram -

76
Q

key features of bacterial invasion

A

feature virulent genes which can be transfered to a host cell
virtical gene transfer : plasmids replicate and create two identical daughter cells
horezontal gene transfer:
bacteria also produce adhesins, form biofilms and some inject effector proteins into host cells
composed of alpha and beta subunits with b subunit binding to specific receptor of host cell

77
Q

how does vibrio cholerae toxin work

A

b subunit bind to ganglioside receptor on the surface of epithelial integine cell. enter in endosome and are transfered to the golgi and endoplasmic reticullum. activate the adenylate cyclase. this creates cAMP from ATP move cl- out of the cell

78
Q

key features of viruses

A

Obligate intracellular parasite, rely on host cell.
Unlike bacteria and eukaryotic parasites, viruses cannot replicate or survive on their own.
They lack the ability to produce the proteins encoded by their DNA or RNA genomes.
Virion when outside the host cell.

79
Q

how do viruses invade cells

A

bind to cell surface receptors and enter host cell by either membrane fission or endocytosis. they replicate and form viral DNA which is coded into mRNA to assemble more viruses whih are them released.
drug resistant
they are host specific recognise specific receptors of specific cells

80
Q

key features of protozoan

A

Protozoans are a diverse group of unicellular eukaryotes.
Some require more than one host to carry out their life cycle

81
Q

key features of protozoan invasion (in trypanosoma cruzi)

A

attach to host cell surface receptors
Ca2- singel encourages lysosome
fusion of lysosome with plasma membrane
invade the cell
T. cruzi must escape from the parasitophorous vacuole to gain access to the host cell cytoplasm, where it can replicate and establish infection
secration of pore forming proteins
lysis of surrounding membrane with release of pathogen into cytosol
The parasite secretes pore-forming protein that disrupts the lysosome membrane, thus allowing it to escape into the host-cell cytosol and proliferate

82
Q

What is Hematopoiesis?

A

the process of hematopoietic stem cells differenciate into mature blood cell types

83
Q

what are the types of mature blood cells

A

red blood cells , granulocytes, macrophages, dentritic cells, lymphocytes

84
Q

Where does hematopoiesis occur?

A

it first occurs in the yolk sac during fetal development. This then occurs in the dorsal aortal and produce multipotent hematopoietic progenitors
mature into adult HSCs in the aortal or in fetal liver
After birth this occurs in the bone marrow
most HSCs are quiescent (dont devide) in the absence of infections

85
Q

Whats different about t cells

A

t cells mature in the thymus

86
Q

what are the primary lymphoid organs

A

bone marrow and thymus

87
Q

secondary lymphoid organs

A

lymph node, spleen, tonsils and peyers patches in the small intestine

88
Q

what is the first responce to infection

A

myeloid cells
neutrophils, basophils and eosinophils are released. N’s released into blood from bone marrow and engulf pathogens like bacteria in phagocytosis.
B’s contain large granules filled with proteins like histamine.
B and E’s are the immune response to parasitic worms
Mast cells Cytoplasmic granules contain histamine &do not mature in the bone marrow but in peripheral tissues such as the skin, connective tissues of various organs
monocytes migrate to tissue in response to infection and differentiate into macrophages

89
Q

what types of response cells are adaptive response

A

b cells, t cells

90
Q

How does pathogens activate innate immune cell?

A

innate immune cells have pattern recognition receptors (PRRs)recognises pathogen-derived molecules known as pathogen-associated molecular patterns (PAMPS).
A host cell doesn’t produce PAMPS therefore immune cells can recognise whether the cell is its own or not. These inamecells activate adaptive immune cells

91
Q

what do dentritic cells do

A

professional antigen presenting cell

92
Q

what are the basic componants of the neurone

A

dendrites, nucleus, cytoskeleton, axon and growth cone

93
Q

how does neurulation work

A

neuroectodermal cells differenciate and thicken into neural plate and the neural plate boarder separates it from the ectoderm.
This bends dorsally and the two ends join forming the neural crest.
Neural tube closes and disconnects the neural crest from the epidermis.
notochord degenerates and forms the nucleus pulposus of invertebrate disks

94
Q

where does CNS and PNS come from

A

CNS from neural tube
PNS from neural crest

95
Q

How is the spacial expression of transcription factors regulated?

A

signal gradients of sonic hedgehog and BPM in the neural tube with both proteins moving down the concentration gradient in opposite directions

96
Q

how do Neural crest-derived stem cells give rise to the peripheral nervous system

A

The Neural Crest (NC) is a transient embryonic structure which appears between the Neural Chord and the future ectoderm during development of the vertebrate embryo.

NC is a stem cell niche

NC cells migrate out of their niche after neurulation and give rise to various cell populations

97
Q

what are the developmental stages of a neuron

A

initiation/ polarisation , pathfinding, target recognition, branching, synapse formation

98
Q

development of Retinal ganglion cells

A

establishment of retinal layers
directional axonal growth
progression into optic nerve,
decision to cross of turn (depending on whether it controls the left or right side of the eye)
honing in on target region
arrival at target
establishment of topographic map

99
Q

what is the chemoaffinity hypothesis

A

cells and fibres of the brain must carry some type of identifying tag, chemochemical in nature, so they are distinguished from one another

100
Q

principles of axon guidence

A

axons are guided by certain processes tht control signl movement
Adhesive substrate cues convey when singals should go and stop

101
Q

How does ephrin control limb patterning

A

The transcription factor LSL induces expression of EphB receptor in the LMCm
Neurons that grow towards the developing limb are repelled the ligand ephrin-B2 and therefore grow towards the ventral side (away from ephrin-B2)
If any of those factors is lost (TF, receptor or ligand), axons are no longer repelled and therefore grow towards the dorsal side

102
Q

how do growth cones grow in their shape

A

Lamellipodia (dynamic membrane sheet) expand in all directions from the centre of the growth cone and are is supported by a network of short, branched actin fibres
Filopodia are formed by tight parallel bundles of F-actin that polymerise at the leading edge, that push the membrane forward in response to an external cue
Parallel bundles of microtubules guide the extension of axonal microtubule bundles

103
Q

What is the extracellular matrix and how is it formed

A

In tissues, a substantial volume is extracellular space, which is filled with a network of secreted macromolecules: the EXTRACELLULAR MATRIX (ECM)
Each tissue will have specialised ECM, adapted for its function.
eg. -connective tissue = elastic matrix

-bone, teeth = calcified matrix

-cornea = transparent matrix

-tendons = ropelike, high tensile strength
104
Q

Key components of the ECM

A

proteoglycans, fibronectin, collagen, elastins and laminin

105
Q

how does filopodia grow through the clutch model

A

there’s no adhesion in the growth stage actin polymerases continuously no force to push the membrane because actin cant generate a force
intergrin recepter binds to laminin
form focal adhesion between growth substrate and growth cone
activation of integrin signaling
this links polymerasing actin to focal adhesion