Grade 11 Bio POH - Updates
Patterns of Inheritance
Interphase:
G1 phase - normal growth phase, organelles start dividing
CHECKPOINT: is the cell functioning normally
S phase - chromatin duplicates
G2 phase - organelles finish dividing
CHECKPOINT: did the chromatin duplicate successfully
Mitosis:
Prophase - chromatin condenses into chromosomes, nuclear membrane starts disintegrating
Prometaphase - spindle fibers appear, start moving to poles of cell
Metaphase - chromosomes start lining up in the middle of cell, spindle fibers attach
CHECKPOINT: did the spindle fibers attach correctly to the centromeres
Anaphase - spindle fibers pull sister chromatids apart
Telophase - spindle disappears and nucleus forms around each set of daughter chromosomes. The nucleus has to be developed immediately or else the chromatids will move which creates genetic disorder
Cytokinesis: cleavage furrow forms, cell plate forms in plant cells as they don't have centrioles so a plate develops using small segments of cellulose
Types of mitosis:
Binary fission - when prokaryotes are tired of dividing, it goes through sexual reproduction. Two prokaryotes will create a tuba made of pili called the conjugation bridge and genetic material will pass through. Then they join together
Fragmentation - the whole organism is broken and the fragments grows into a new organism
Vegetative propagation - only a small part of the plant is broken which will grow into a whole new plant
Budding - budding is when there is an outgrowth and it falls of and grows into a whole new plant
What makes mitosis work:
Cyclins are proteins (g1 cyclin, g1/s cyclin, s cyclin, m cyclin)
Intermolecular signals that regulate and drive mitosis (proto oncogene)
They must be activated by a CDK (cyclin dependent kinase) to create a cyclin-CDK complex.
When this happens the CDK is activated and can modify phosphorylated target proteins
The CDK attaches phosphates to the target protein which acts like a switch making it more or less active
So when they attach, the cyclin activates the CDK but also directs the CDK to target proteins (depending on the stage of the cycle)
And then based on the type of cyclin and target protein, the specific stage starts
MPFs (m phase promoting factor)
Researchers found that cells in m phase had a mystery substance that could force g2 frog cells to go into m phase
This was just CDK attached to a M cyclin
During interphase, M cyclin stays low but builds up as it approaches m phase
As m cyclin builds up, it binds to the already present CDKs and the complex triggers m phase
If the cyclin lvl is too much, the cell divides out of control
MPF triggers it's own destruction by activating the anaphase promoting complex/cyclosome (APC/C)
Protein that causes m cyclins to be destroyed starting in anaphase
When this happens the cells gets pushed out of mitosis
APC/C also destroys the protein holding sis chromatids together which helps them separate in anaphase
They respond to cues from the environment in and out the cell
Growth factors: positive cues that are released from other cells. They stimulate the synthesis of cyclin
Density dependent inhibition: negative cues that say that if there are too many cells in the area, they will compete and it will cause a tumor
Other regulators:
Cell checkpoints
Proto oncogenes (cyclin-CDK or MPF or APC)
Start cell division, essential for cell development
Tumor suppressor genes (p53)
Switch of cell division
P53 is a gene that encodes a protein that halts the cell cycle so that DNA can be repaired for division
What happens if one of the checkpoints fails?
P53 commands other genes to bring cell division to a halt
If the damage is too serious for repair, p53 activates other genes to cause the cell to go through apoptosis
If repairs are made, p53 allows the cell cycle to continue
G0 phase and differentiation:
When cells exit mitosis or it's not necessary for them to divide, the enter g0 phase where normal cell functions continue but they don't go through m phase
They can stay here for years or never leave
Cells might stop dividing to get jobs in structure and function this is known as differentiation
They differentiate from stem cells
Cancer:
Too much cell division or too little cell death
If the APC gene is mutated, the cells will pile up creating a tumor
Cancerous cells do not obey checkpoints or regulators so there is no density dependent inhibition
Proto oncogenes require one allele (different ver of same gene) to be mutated and they are considered dominant resulting in a gain of function
tumor suppressor genes require one allele to be mutated and they are considered recessive resulting in a loss of function
Considered immortal as long as oxygenated blood is available
Angiogenesis - creation of new blood vessels to feed tumor
Telomerase - enzyme that fuels the abnormal production of cyclin
Telomerase is needed during development of the womb to make an organism develop faster but one it is developed, it gets turned off normally
Gets turned back on because of carcinogens
Tumors
Benign - encapsulated, non invasive, not deadly, can be removed
Malignant - invasive, grows between cells destroying issue, deadly, treated with chemo, radiation, surgery
Metastasis - movement of cancer cells
Travel through blood vessels or lymph tracts. It cannot grow in the heart, it's too hard and blood moves too quickly.
Accumulation of mutations over a lifetime
We all have oncogenes in our genome but some ppl have stronger control mechanisms that resist mutations some have weaker
Signaling molecules:
Stages
Reception
signaling molecule binds to membrane receptor protein
Receptors and ligands are personalized to the cell
Transduction
Amplifies the signal
Signal transduction pathway - The chains of molecules that relay intracellular signals
Powered by phosphorylation
Response
Action is carried out
Different ligands and receptor combinations carry out different responses
Eukaryotic signaling
Autocrine - cells produce a hormone or chemical messenger to react to their own signals
Regulates cellular growth and development
Important in cancer, plays a key role in metastasis
EXAMPLE: presence of foreign antibody causes T-cells to produce a growth factor to stimulate their own production which fight the infection
Paracrine - cells communicate over short distances and use diffusion
Ligands diffuse of signal cell by exocytosis and then binds to receptors outside of a nearby cell
The gap between the signal cell and target cell is called the synapse
allows cells to locally coordinate activities with other cells
important during development, when they allow one group of cells to tell a neighboring group of cells what cellular identity to take on
EXAMPLE: neurotransmitters released from a nerve cell travel across the synapse to another cell to cause a response
Endocrine - long distance signaling uses the circulatory system
Involve hormones released from endocrine glands or cytokines
EXAMPLE: insulin within pancreas stimulates the uptake of glucose within cells (decreasing blood sugar levels). Glucagon is another hormone that triggers glycogen to convert into glucose and to enter your bloodstream so that your body can use it for energy
Cell-to-cell contact
Gap junctions in animals and plasmodesmata in plants
Water filled channels that allow intracellular mediators to diffuse between cells
transmits the current state of one cell to its neighbor so a group of cells can coordinate their response to a signal that only one of them may have received
EXAMPLE: plasmodesmata
Complementary proteins on the surfaces of both cells bind together
Interaction changes the shape of one of both proteins which transmits a signal
EXAMPLE: in immune cells they use cell surface markers to recognize self cells and cells infected by pathogens
Pheromones - chemical signals excreted into the environment to cause a response in other organisms
Affect the behavior of members of the same species
EXAMPLE: bombykol is released by female silk moths and is detected in low concentrations by males. The binding protein on males antennae binds the bombykol which triggers a wing fluttering movement to locate the mate.
An intracellular signaling could look like this:
A steroid molecules goes into the cell and binds to a protein receptor inside the cell and becomes active
P.R travels to the nucleus where it binds to DNA and can get transcription of a certain gene going which can encode a protein
Prokaryotic Signaling:
Quorum sensing
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Meiosis:
3 possible types of cell cycles based on DNA content
Alternation of generations
Half and half diploid and haploid
Plants and most algae
Diploid majority:
In animals
Haploid majority:
Fungi and some prokaryotes
Spend most of their lives with haploid cells
Come together to make diploid cells to create variation
After recombining, they undergo meiosis to return to a haploid state but with different DNA composition
General info
Locus: where a gene is located
Alleles: different versions of the same gene (e.g. two genes both encoding for height but one gene encodes for short and another encodes for tall)
Genotype/genome: a complete set of genes (the entire genetic makeup)
Phenotype: observable traits resulting from the genotype
Heredity: transmission of traits from one generation to the next
Most DNA is for common information (e.g. blood)
Some DNA is for varied information (diversity amongst species)
Genetics: science that deals with the transmission of info in the form of DNA
Gene: unit of heredity info
Benefits of sexual reproduction: creates variation, means there exists the possibility to evolve over time in a changing environment
Risks: not good for endangered species it takes more time and is complicated
Meiosis 1: reduction division because the number of chromosomes in the parent cell will be less in the daughter cells
Prophase 1
chromosomes come close in pairs of homologous chromosomes. When they come close this is called synapsis which creates a tetrad of chromosomes (2n = 4, 8 sister chromatids)
The pairs crossing over, exchanging genetic information aka recombination. The point where they cross over is known as the chiasma(ta)
The only exception to this is in XY chromosomes, they only join at the tips
Nuclear membrane dissolves
Metaphse 1:
The pairs of chromosomes line up in the middle of the cell side by side and the spindle fibers attach to the centromeres of the pairs of sister chromatids
Anaphse 1
The pairs separate so opposite poles
Telophase 1
nuclear membrane forms and cytokenises happens, making 2 different daughter cells
Result: 2 non identical daughter cells with 23 chromosomes
Meiosis 2: mitosis
Result: 4 non identical daughter cells with 23 chromosomes
Gametogenesis:
How is genetic variety possible?
crossing over/recombination
independent assortment: metaphase and anaphase
Random fertilization
Oogenesis: making of one egg cell
At the end of mitosis, you have 2 oogoni(a)um
After they go through recombination, they become primary oocyte
In cytokinesis 1, the division is not equal and one of the daughter cells is much more bigger than the other
The bigger daughter cell is a secondary oocyte and the smaller daughter is a polar body
The secondary oocyte creates 2 daughter cells, one will be bigger known as an egg and the other is just a polar body
The polar body from before creates 2 polar bodies
In the end, there's only one egg cell made
Spermatogenesis: making of sperm cells
At the end of mitosis, you have 2 spermatogoni(a)um
After they go through recombination, they become primary spermatocyte
The resulting haploid daughter cells are called secondary spermatocyte
After they go through meiosis 2, the resulting daughter cells are spermatids and all of them develop into sperm
Nondisjunction
Abnormal chromosome number
Aneuploidy - a cell can have one or a couple of chromosomes missing
polyploidy - extra complete sets of chromosomes
Monosomy - fertilization involves a gamete that is missing a chromosome (45)
Polysomy - fertilization involves a gamete that has one extra chromosome (47)
Trisomy - fertilized egg has triplicate chromosomes (2n+1) e.g. Trisomy 21 is down syndrome so the 21st pair of a karyotype has one extra chromosome
In meiosis 2/mitosis, the resulting cells will have n+1, n-1, n and n if there are 2 other cells
In meiosis 1, the resulting cells will have n+1 and n-1
Karyotype notation - #of chromosomes, sex, which pair the problem is (in down syndrome it's (47,XX,+21))
Abnormal chromosome structure
Deletion: segments exchanged involve a bigger segment being exchanged for a smaller segment, therefore nucleotides are lost and genetic information is also lost. Lethal if essential genes are missing
Cri-du-chat syndrome is loss or genetic misplacement from the 5th chromosome. The crying sounds like a cat crying
Duplication: two or more copies of the same DNA is produced
Pallister killian syndrome is where the 12th chromosome is duplicated. developmental delay, intellectual disability, recurrent infections, seizures
Inversion: a segment breaks off and reattaches within the same chromosome, but in reverse orientation
Hunter syndrome. Clouding of the front part of the eye, respiratory infections, Enlarged tonsils and distinct facial features
Translocation: a piece of one chromosome breaks off and attaches to another chromosome
Translocation Down syndrome three # 21 chromosomes, just like there are in trisomy 21, but one of the 21 chromosomes is attached to another chromosome, instead of being separate
Syndromes
Cri-du-chat
Karyotype: 46XX or 46XY
5th chromosome deletion
Cry which sounds like that of a cat in distress because the larynx is improperly developed
Small cranium, small jaw, moon-shaped face
Deletion of half the short arm of chromosome number 5
Patau syndrome
Karyotype: 47XX or 47XY
13th chromosome trisomy
Abnormal cerebral functions, death in early infancy, pronounced clefts of the lip and plate, broad nose, polydactyly, small cranium, dysfunctional eyes, heart defects, neurological challenges
Edwards syndrome
Karyotype: 47XX or 47XY
18th chromosome trisomy
Severe neurological challenges, elongated skull, narrow pelvis, rocker bottom feet, malformed heart, grasping of the two central fingers by thumb and index
Down syndrome
Karyotype: 47XX or 47XY
21st chromosome trisomy
Short stature, broad hands, stubby fingers and toes, a wide rounded face, a large tongue (hard to talk), neurological challenges
Prone to respiratory infections, leukemia, and heart defects
Jacobs
Karyotype: 47XYY (extra Y)
Nondisjunction of the Y chromosome during meiosis
ONLY IN MEN
Tall, develop heavy acne, neurological challenges
Klinefelter
Karyotype: 47XXY or 47XXXY (1 or 2 extra X)
Tall stature, small testicles, developed breasts, sterility
ONLY IN MEN
Turner Syndrome
Karyotype: 45XXX or 45X
X carrying sperm fertilized an ovum that lacks an X
Or when sperm lacking an X or Y fertilizes an X egg
ONLY GIRLS
Short, chunky build, webbed neck, no menstruation, no breast development, sterile
Triple X
Karyotype: 47XXX
ONLY GIRLS
Underdeveloped genitalia and limited fertility
Neuromotor delays
Mendelian Genetics - Laws of inheritance
Mnedel’s Law of Dominance
Only one of the two alleles from one of the parents is present and expresses itself in the offspring
Mendel’s Law of Independent Assortment
Inheritance of one pair of alleles is independent of inheritance of another pair of alleles
the alleles of two (or more) different genes get sorted into gametes independently of one another
Mendel’s Law of Segregation
An individual possesses two alleles - one from each parent
during meiosis,allele pairs segregate and re-unite randomly during fertilization
After Mendel Genetics or Non-mendelian traits
COMPLETE DOMINANCE
Mendelian genetics, only one out of the two alleles are expressed
INCOMPLETE DOMINANCE (or blending inheritance)
The genetic info is blended together (red+white = pink)
Neither phenotype is completely dominating
CODOMINANCE
Both alleles are expressed (speckled cows)
POLYGENIC INHERITANCE
Multiple alleles code for a phenotype (height, skin tone)
Happens because of quantitative characters
Skin color depends on how many copies of the same genes for making melanin you inherited from your parents
EPISTASIS
One gene depends on another gene to be expressed
Several genes interact to create the phenotypes of hair (texture, thickness, color)
Phenotypic expression is reduced which is why there is a 9:3:4 ratio opposed to the normal 9:3:3:1 ratio
Multiple Alleles
Multiple versions of the same allele
Blood cells have proteins on their surface that are called antigens which trigger an immune response if foreign to the body (A, B, AB, or O)
If type B blood was donated to a person who had type A blood, it can lead to shock or clumping which is fatal because the white blood cells begin killing the new blood cells
Type O is a universal donor because it has NO antigens
Type AB is a universal receiver because it has BOTH antigens
If the blood type has a +, the blood cell has a protein called the RH factor
If the blood type has a -, the blood cell does not have an RH factor
BLOOD TYPE IS INHERITED!!!
Epigenetics:
Field of research showing how environmental influences have an impact on genes
Nature vs Nurture are both 50-50
Epigenome
Collection of chemical marks on DNA that determine gene expression
The experiences of children can change the epigenome which explains why identical twins can develop differently
Experiences affect how information is released by genes even though inherited genes provide the information
Twin Study
Compare monozygotic (identical - fertilized egg splits into two) and dizygotic (fraternal - two separate eggs are fertilized by two separate sperm) to estimate how genetics are influenced by the environment
IT share 100% of genes but FT only share 50% so researches can compare them
Twin studies rely on two main assumptions:
Equal environments: Identical and fraternal twins experience equally similar environments
Little or no assortative mating: People don't tend to choose partners similar to themselves
Twin studies have shown genetic influences on many traits like schizophrenia, personality, cognitive skills, etc. They estimate heritability as well as shared and unshared environmental influences.
Advances in molecular genetics have largely supported findings from twin studies, validating them as an exploratory tool.
Twin studies remain valuable even with DNA-based research
Twin studies are still important for studying complex traits where specific genes are hard to identify
Explore potential genetic bases of traits
Estimate trait expression in people with certain genes (using identical twins)
Provide age-matched samples for genetic mapping (using fraternal twins)
They can help examine gene-environment interactions by comparing heritability estimates across different environments.
Twin studies complement molecular genetics and social science in understanding how genes and environment combine to influence human traits and behaviors.