Processes Flashcards
Meiosis 1
The chromosomes that replicated prior to meiosis 1, EACH consist of 2 genetically identical chromatids attached at the centromere.
The chromosomes condense and the homologous chromosomes pair up.
Chiasmata form at points of contact between the non-sister chromatids of a homologous pair and sections of DNA are exchanged.
This crossing over of DNA is random and produces genetically different recombinant chromosomes.
Spindle fibres attach to the homologous pairs and line them up at the equator of the spindle.
The orientation of the pairs of homologous chromosomes at the equator is random.
The chromosomes of each pair are separated and move towards OPPOSITE poles.
Cytokinesis occurs and 2 daughter cells are formed.
Meiosis 2
Each of the 2 cells produced in Meiosis 1 undergoes further division, during which the sister chromatids of each chromosome are separated.
Sodium Potassium pump
The pump has its ion binding sites exposed to the cytoplasm and there is a high affinity for Na+. So binding occurs.
This causes phosphorylation by ATP, resulting in the pump changing conformation.
The pump has its ion binding sites exposed to outside to the cell. The affinity for Na+ is low and so the Na+ are released out of the cell.
There is a high affinity for K+, so binding occurs from out of the cell.
This triggers de phosphorylation of the pump.
The pump returns to the original conformation with its binding sites exposed to the cytoplasm. There is a low affinity for K+, and so they are taken into the cell.
Now the affinity returns to the start.
Hydrophobic signalling
Hydrophobic signalling molecules diffuse through the phospholipid bilayer.
The molecule binds to transcription factors in the cytosol.
The hormone-receptor complex moves to the nucleus.
The complex binds with specific sequences of DNA.
This affects gene expression.
Hydrophilic Signalling
The hydrophilic signalling molecule binds to transmembrane receptors. They DO NOT enter the cytosol.
The transmembrane receptors change conformation when the ligand binds to the extra cellular surface.
The signal molecule does not enter the cell.
The signal is transduced across the plasma membrane.
Transmembrane receptors act as signal transducers, converting the extra cellular ligand binding event into intracellular signals.
This alters cell behaviour.
Nerve Impulse Transmission
Neurotransmitters bind to receptors (ligand gated channels) at a synapse.
This causes the ligand gated channel to open, so Na+ diffuses into the neuron.
This Na+ movement causes depolarisation of the plasma membrane.
This depolarisation reaches a critical threshold level.
Voltage gated channel opens, so the Na+ diffuse into the neuron down the electrochemical gradient.
This causes a wave of electrical excitation along the neurons plasma membrane.
The voltage builds up and so the Na+ channel is inactivated and the K+ channel opens .
The K+ diffuse out of the neuron, resulting in repolarisation.
Resting potential is restored, so the K+ channels close and the Na+ channels are ready.
Electrochemical gradient is reset.
Rod cells
Retinal absorbs a photon of light which causes it to change shape.
In turn rhodopsin changes conformation to become photoexcited rhodopsin.
A cascade of proteins amplifies the signal.
Photo-excited rhodopsin activates a G protein called transducin which activates the enzyme phosphodiesterase.
Phosphodiesterase catalyses the hydrolysis of a molecule called cyclic GMP.
This causes closure of the ion channels in the membrane of Rod cells.
This triggers nerve impulses in the neurons in the retina.
A very high degree of amplification results in rod cells being able to respond to low intensities of light.
Natural Selection
Populations produce more offspring than the environment can support.
Individuals with mutations that best fit their environment are more likely to survive longer and produce more offspring.
Breeding occurs and alleles that confer an advantage are passed on to the next generation.
X chromosome inactivation
In homogametic females (XX) one of the 2X chromosomes present in each cell is inactivated RANDOMLY at an early stage of development.
X chromosome inactivation prevents a double dose of gene products which could be harmful to cells.
Carriers are less likely to be affected by any delirious mutations on these X chromosomes.
As the X chromosome inactivated in each cell is random, 1/2 the cells in any tissue will have a working copy of the gene in question.
Viral Life Cycle Stages
Viral antigens attach to the host cell
Viral DNA is injected into the host cell
Viral DNA is replicated by host cell enzymes
Viral genes are transcribed to RNA which is translated to make viral proteins
New viral particles are assembled and released
Non-specific defence against parasitic attack
First line defences are PHYSICAL BARRIERS and CHEMICAL SECRETIONS, that work together to prevent parasites from entering the bodily fluids.
Second line defences ( INFLAMMATORY RESPONSE, PHAGOCYTES and NATURAL KILLER CELLS) happen as a response after a parasite has entered the bodily fluids.
Inflammatory response
Histamine is released
Triggers dilation of blood vessels (enhancing blood flow to area)
Increased permeability of blood vessels
Causes swelling
Stimulates phagocytes to migrate to the area
Phagocytosis
Phagocytes engulf and digest the foreign object using powerful enzymes contained in the lysosomes
Natural killer cells
Type of white blood cell
Detect abnormal cell-surface proteins found on virus-infected cells / cancerous cells
Attach to the stricken cell & release chemicals into it
The chemicals induce cell death
Phagocytes engulf and digest the resulting cell debris
Specific defences against parasitic attack
A range of white blood cells constantly circulates, monitoring the tissues.
If the tissues become damaged or invaded, cells release CYTOKINES that increase blood flow
This results in non-specific and specific white blood cells accumulating at the site of infection or tissue damage.