8 Cells And How They Replicate Flashcards
Prokaryotes - Nucleus
No nucleus, DNA in nucleoid region
Eukaryotes - nucleus
True nucleus with a nuclear membrane
Prokaryotes - DNA structure
Generally circular, single chromosome
Eukaryotes - DNA structure
Multiple linear chromosomes within nucleus
Prokaryotes - membrane bound organelles
Absent
Eukaryotes - membrane bound organelles
Present (eg. Mitochondria and chloroplasts)
Prokaryotes - cell division
Binary fission
Eukaryotes - cell division
Mitosis and meiosis
Prokaryotes - size
1-10 um
Eukaryotes - size
10-100 um
Prokaryotes - metabolic diversity
High (including extremophiles)
Eukaryotes - metabolic diversity
Limited (autotrophic or heterotrophic)
Prokaryotes - cell wall composition
Common - peptidoglycan in bacteria
Eukaryotes - cell wall composition
Variable - cellulose in plants, chitin in fungi
Prokaryotes - ribosome
Smaller 70S
Eukaryotes - ribosome
Larger 80S in cytoplasm
Smaller 70S in mitochondria and chloroplasts
Case study - treating bacterial vs fundal infections (A Cellular Approach)
Bacterial and fungal infections are common in healthcare / community
Require different distinct treatments - successful treatment relies on understanding cellular biology of the pathogen and that of the host
Bacteria vs Fungi
Bacteria - prokaryote
Fungi - eukaryote
B - primary asexual reproduction
F - sexual and asexual through spores
Cell wall composition - bacteria composed of peptidoglycan and the fungi wall is composed of chitin
How do AB treatments work (7)
- Cell wall synthesis inhibitors —> beta laxtams / glycopeptides / fosfomycin / bacitracin / alafosfalin
- DNA gyrase inhibitors - quinolones / coumermycin antibiotics
- Inhibition of DNA dependany RNA polymerase —> Rifampicin
- RNA synthesis inhibitors —> ansamycines
- Protein synthesis (30S and 50S) —> tetracyclines
- Folate synthesis inhibitors —> sulfonamides
- Cell membrane synthesis disruptors —> lipopeptides
Case scenario - treating a patient with dual infections
Choose appropriate antibiotics and anti-fungals without causing harm or drug resistance
Case scenario - treating a patient with dual infections (implications for medical practice)
Distinguishing between cell types matters in clinical settings
Accurate diagnosis and undertsanding of cellular biology it’s important in preventing treat,ent failures, drug resistance and unnecessary dysbiosis in the host
Parasitic infections
Eukaryotic share some cellular structures with human cells / difficult to develop drugs that selectively target the parasite
Cancer treatment
Cancer cells are eukaryotic But exhibit abnormal cell division and structural characteristics - some drugs target specific structures in cancer cells, such as rapidly dividing DNA, mutates protein receptors, or overexpressed enzymes
Understanding cancer cell structure and behaviour allows for the development of targeted therapies that aim to reduce harm to normal cells
Autoimmune diseases
Immune system targets own body cells —> treatment focuses on modulating the immune system
Helps prevent damage to healthy cells
Antibiotic selection in multi-drug resistant bacterial infections
Bacteria can develop resistances to break down the drugs (eg. Resistance to penicillin by producing enzyme beta-lactamase)
Requires the use of alternatives
Testing to determine what the bacteria is sensitive to
Bacterial ribosome composition
70S (composed of 30S and 50S subunits)
Eukaryote ribosome composition
80S (composed of 40S and 60S subunits)
Why do some antibiotics target bacterial ribosomes
Antibiotics like tetracycline and erythromycin specifically bind to the bacterial subunits (either 30S or 50S), disrupting protein synthesis
These antibiotics prevent bacterial cells from making essential proteins, ultimately inhibiting growth or leading to cell death
Why don’t antibiotics harm human cells?
Human cells have 80S ribsomones with different structural characteristics, so these antibiotics don’t recognise or bind to them effectively
Structural specificity means antibiotics can selectively inhibit bacterial cells without harming eukaryotic cells
Examples of common ribosome targeting antibiotics - tetracycline
binds to the 30S subunit, blocking tRNA from attaching and halting protein synthesis
Examples of common ribosome targeting antibiotics - erythromycin
binds to the 50S subunit preventing the ribosomes from moving along mRNA, stopping protein production
Examples of common ribosome targeting antibiotics - Streptomycin
binds to the 30S subunit causing misreading of mRNA and resulting in faulty proteins
Summary - Antibiotics targeting ribosomes
Selective targeting - antibiotics can selectively bind to bacterial ribosomes without affecting eukaryotic ribosomes
Structural differences in ribosome size and subunit composition is crucial for this selective effect
Implication for treatment - this selectivity allows antibiotics to combat bacterial infections without generally harming human cells
