Gene Expression Flashcards
define stem cell
undifferentiated cells that continually divide and become specialised
different types of stem cells
totipotent-can divide and produce any type of body cell, they occur only for a limited time in early mammalian embryos.
pluripotent-found in embryos (from the inner mass of a blastocyst), can differentiate into any type of cell excluding placenta and embryo.
multipotent- can only differentiate into a limited number of cells, found in mature mammals e.g in bone marrow + only differentiates to different blood cells
unipotent- can only differentiate to form one type of cell, lots of genes are switched off by regulation of transcription factors, found in mature mammals.
uses of embryonic stem cells- pluripotent + its benefits
due to their potency, they can be used to research using them to treat human disorders by growing new organs and tissues e.g Parkinson’s disease or spinal cord injuries.
-this saves or improves quality of life for many people, reduces the need for organ donation
issues with using embryonic stem cells
-sometimes the treatment doesn’t work, or the stem cells continually divide to create tumours.
-ethical issues: whether it is right to make a therapeutic clone of yourself to get stem cells from embryo then destroy it
fertilised egg- embryo is a potential life being destroyed
sources of stem cells
-embryos: contain stem cells that are pluripotent
-umbilical cord blood: contains stem cells that are multipotent
-placenta: multipotent stem cells
-adult stem cells: multipotent, produce different stem cells to repair those within a particular tissue or organ
what happens to totipotent cells during embryonic development
certain parts of the DNA are selectively translated so that only some genes are “switched on”,in order to differentiate the cell into a specific type and form the tissues that make up the foetus.
unipotent stem cells with example
-a cell that only develops into one type of cell
-happens at the end of specialisation, when the cell can only propagate its own type
-e.g. cardiomyocytes can divide to form other heart muscle cells
uses of stem cells
-medical therapies e.g bone marrow transplants, treating blood disorders
-drug testing on artificially grown tissues
-research e.g. the formation of organs and embryos
what are induced pluripotent stem cells (iPS cells)
prouced from mature, fully specialised (somatic) adult cells using appropriate protein transcription factors to overcome some of the ethical issues regarding use of embryonic stem cells.
-have pluripotent state that enables the devlelopment of an unlimited source of any type of human cell needed for therapeutic purposes.
how are iPS cells produced
-created from adult unipotent cells, which are altered in a lab to return them to state of pluripotency.
-to do this genes that were switched off to make the cell specialised are switched back on by transcriptional factors
-very similiar to pluripotent embryonic stem cells, but does not cause the destruction of an embryo & the adult can giver permission
transcription factor
protein that controls the transcription of the gene so that only certain parts of the DNA are expressed -> in order to allow a cell to specialise.
difference between activator and repressor
activator-a transcription factor that increases rate of transcription.
repressor- a transcription factor that decreases the rate of trancription.
how do transcription factors work
-moves from the cytoplasm into the nucleus
-it binds to the promoter region upstream of target gene
-this makes it easier or more difficult for RNA polymerase to bind to gene. This increases or decreases rate of transcription.
role of oestrogen
-oestrogen is a steroid hormone that can initiate transcription
-it diffuses through cell membrane
-it binds to receptor site on transcriptional factor
-when it binds to the transcriptional factor it causes it to change shape slightly
-this change in shape makes it complementary and bind to the DNA to initiate transcription.
epigenetics
the heritable change in gene function, without changing the DNA base sequence.
-caused by changes in environment and can inhibit transcription.
environmental factors that can affect epigenetics
factors such as diet, stress and toxins can add epigentic (chemical tags) to the DNA and this can control gene expression.
epigenome
the single layer of chemical tags on the histone proteins which are associated with DNA
-these determine the shape of the histone-DNA complex and whether the DNA is tightly wound or unwound->help control the transcription of genes
-if DNA is tightly wound, transcription factors cannot bind, therefore the epigenome, due to changes in environment, can inhibit transcription.
2 ways epigenetics can control gene expression
-increasing methylation of DNA
-acetylation of histones
how does increased methylation of DNA affect gene transcription
-involves adding methyl (CH3) to cytosine bases on DNA using DNA methyl transferase enzymes.
-this alters the DNA structure-condenses the DNA-histone complex, preventing transcriptional factors from binding to it
-gene transcription is inhibited
how does increased acetylation of histones affect gene transcription
-negatively charged acetyl groups repel each other, the DNA loosens from the histones making it less condensed-> makes it more accessible for transcriptional factors to bind.
how does decreased acetylation of histones affect gene transcription
-decreased acetylation of associated histones on DNA inhibits transcription.->increases the positive charge of histones, so attracted to more phosphate groups on DNA.
-binding becomes too tight and prevents transcription factors from accessing the DNA.
-gene transcription is suppressed.
how can epigenetics cause disease
-by overactivating a gene’s function (such as in cancer) or by suppressing it.
application of epigenetics
-used for treatment of various diseases
-development of ways to reverse epigenetic changes
role of tumour suppressor genes + how it can lead to cancer
-these genes code for proteins that slow down cell division, repair DNA mistakes and cause cell death-apoptosis-if DNA copying errors are detected.
-if a mutation occurs, or due to epigenetics and results in tumour suppressor gene not producing the proteins to carry out this function-cells can grow out of control, mutated cells would not be identified and destroyed which can lead to cancer
abnormal methylation
-abnormal methylation of proto-oncogenes and tumour suppressor genes can cause abnormal cell growth and cancers develop:
-hypermethylation of tumour suppressor genes->increased number of methyl groups attached to it, resulting in gene being inactivated and becomes turned off-can cause cells to divide uncontrollably by mitosis and form tumours
-hypomethylation of proto-oncogenes->reduces the number of methyl groups attached, causing them to be permanently switched on-producing proteins that encourage cell division
RNA interferance (RNAi)
-small lengths of non-coding RNA, regulate gene expression by affecting translation, prevents mRNA that has already been transcribed from being translated into a protein.
-occurs in eukaryotes and some prokaryotes.
two types of RNAi
-short interfering RNA (siRNA): in animals only
-micro RNA (miRNA): in plants and animals
process of RNAi
-an enzyme is used to unwind the double stranded siRNA in cytoplasm
-one of the siRNA strands is used, while other degrades (breaks down).
-the siRNA combines with an enzyme->siRNA-enzyme complex
-the siRNA-enzyme complex binds to target mRNA (as it is complementary to the ase sequence in a section).
-the enzyme with siRNA cuts the mRNA into small fragments- so it can no longer be translated
cancer
the result of mutations in genes that regulate mitosis
if these genes mutate and non-functioning proteins are made then mitosis is not regulated-resulting in the uncontrollable cell division of cells and creation of tumour.
benign tumours
-slow growth
-non cancerous-> defined by a clear boundary due to cell adhesion ( sticking them together)
-cells retain function and normal shape
-don’t spread easily
-easy to treat
-often not life-threatening, depending on tumour location e.g. in brain-alot harder to remove without damaging brain tissue
malignant tumour
-rapid, uncontrollable cell division
-cell nucleus becomes large, cell can become unspecialised again
-don’t produce adhesive, metastasis occurs-> spreads quickly and easily
-finger-like projections into surrounding tissue and develop its own blood supply
-can be life-threatening: much harder to remove tumours, recurrance is more likely
role of proto-oncogenes + how it can lead to cancer
-proto-oncogenes code for proteins involved in initiation of DNA replication and mitosis cell division when the body needs new cells.
-mutation can occur- producing mutated version-> oncogene: become permanently activated, cells grow out of control, dividing continually leading to formation of tumours
how can oestrogen be involved in developing breast cancer
-increased oestrogen concentrations can lead to breast cancer as:
-post-menopause fat cells in breast tissue produce oestrogen instead of in ovaries
-with age, levels of oestrogen present in women’s breast increases
-this can stimulate more breast tissue cells to divide as oestrogen is an activator of RNA polymerase, increasing chance of mutation
-cancer cell replication could be further promoted by oestrogen causing faster tumour growth.
