Cell Physiology Study Guide - Eukaryotes and Prokaryotes

Animal cells

Phospholipid bilayer, cholesterol, no cell wall.

Fungal cells

Cell wall (chitin & β-glucan), membrane contains ergosterol (antifungal target).

Protista

Flexible membrane; cyst forms may have walls.

Organelles in eukaryotes

Nucleus, mitochondria, ER, Golgi, lysosomes, peroxisomes.

Microfilaments (actin)

Movement & shape.

Intermediate filaments

Support.

Microtubules

Strength, replication, transport.

Animal cell replication methods

Mitosis (somatic), meiosis (germ cells).

Fungal replication methods

Asexual (budding, mitospores, binary fission) & sexual (gametes → zygospores).

Protista replication methods

Binary/multiple fission, budding, conjugation (varies by species).

Mitosis

One 2n → two 2n cells (identical).

Meiosis

One 2n → four n cells (unique); involves crossing over during prophase I.

Cell cycle checkpoints

Checkpoints at G1-S, G2-M, and spindle assembly.

Cyclins and CDKs

Regulated by cyclins + CDKs (phosphorylate proteins).

p53 role

Halts cycle for DNA repair → mutations here = cancer.

Eukaryotic embryo development stages

Fertilization → zygote → morula → blastocyst → gastrulation → organogenesis.

1st trimester development

Most major structures.

2nd/3rd trimester development

CNS development & growth.

Cellular differentiation

Controlled by gene expression, driven by signal transduction and pattern formation.

Types of stem cell potency

Totipotent: any cell (zygote). Pluripotent: many types. Multipotent: few (e.g., blood). Unipotent: one type.

Signal transduction process

Ligand → receptor → G protein → adenylate cyclase → cAMP → CREB → nucleus → gene transcription.

Impact of drugs on signal transduction

PDE inhibitors (e.g., sildenafil) prolong cAMP activity. Clopidogrel inhibits signaling in platelets.

Three germ layers

Ectoderm: skin, nervous system. Mesoderm: muscle, bone, blood. Endoderm: gut lining, lungs, liver.

Congenital abnormalities

Arise from errors in morphogenesis, cell migration, or differentiation.

Fungal cell composition

Cell wall: chitin & β-glucan. Membrane sterol: ergosterol (drug target). No peptidoglycan → insensitive to antibiotics.

Fungi habitat

Soil, bird feces (Histoplasma, Cryptococcus), vegetation (Aspergillus). Some are regional (e.g., Coccidioides in Southwest USA).

Candida albicans

overgrows after antibiotics or skin damage → thrush, vaginitis.

Animal metabolism

obligate aerobes; lactic acid in hypoxia.

Fungal metabolism

mostly aerobes; some ferment → ethanol.

Protista metabolism

obligate aerobes or anaerobes; anaerobes → lactic acid.

Fungal forms

Yeasts, molds, dimorphic forms.

Protista forms

trophozoites (active), cysts (transmission form).

Animal locomotion structures

pseudopodia, cilia, flagella.

Protista locomotion structures

same as animals, plus kinetoplast (flagellar motor).

Free-living protista encystment

encyst during stress (dry, no food).

Parasitic protista encystment

cysts outside host → excyst inside host.

Trophozoite

active, metabolizing in host.

Cyst

dormant, environmental transmission.

Typical parasite life cycle

Sporozoite → gametocyte → mating → ookinete → oocyst → new sporozoites.

Definitive host

where sexual reproduction occurs (e.g., cats for Toxoplasma).

Intermediate host

asexual stages (e.g., humans ingesting oocysts).

Bacterial shapes

Cocci (spherical) → Staphylococcus, Streptococcus; Bacilli (rod-shaped) → E. coli; Spirochetes (spiral) → Treponema pallidum; Pleomorphic → variable shape.

Bacterial arrangements

Diplo (pairs), Strepto (chains), Staphylo (clusters).

Prokaryotic membrane composition

phospholipid bilayer, no sterols (except Mycoplasma).

Bacterial cell wall

peptidoglycan (NAG + NAM) → targeted by antibiotics (e.g., β-lactams).

Eukaryotic membrane composition

cholesterol-based membrane, no peptidoglycan.

Prokaryotic ribosomes

70S (50S + 30S), smaller than eukaryotic 80S.

Prokaryotic genomes

single circular DNA, no nucleus or histones.

Plasmids

extra-chromosomal DNA, often carry resistance/toxin genes.

Transposons

mobile DNA; can insert into various sites, disrupt genes.

Plasmids as virulence factors

Encode toxins, pili, antibiotic resistance (e.g., β-lactamase), enzymes, bacteriocins.

Transposons as virulence factors

Move virulence genes between plasmids or chromosomes, cause mutations.

Bacterial capsule

antiphagocytic, serotype identifier, vaccine target.

Glycocalyx

slime layer for adhesion → biofilms.

Pili (fimbriae)

adhesion to host cells, sex pilus for conjugation.

Flagella

motility, chemotaxis, antigenic identification.

Spores

Form in stress (low nutrients) by Clostridium, Bacillus. Resistant: to heat, radiation, chemicals. Contain DNA, minimal water, keratin-like coat.

Human diseases caused by spores

Cause tetanus, anthrax, botulism. Cannot be killed by boiling → need autoclaving (steam under pressure).

Gram positive bacteria

Thick peptidoglycan, teichoic acid, purple stain (e.g., Staph, Strep).

Gram negative bacteria

Thin wall + outer membrane with LPS, pink stain (e.g., E. coli, Pseudomonas).

Acid-fast bacteria

Mycolic acid in wall → waxy coating. Stained with Ziehl-Neelsen (carbolfuchsin). Examples: Mycobacterium tuberculosis, M. leprae.

Bacteria that cannot be Gram stained

Dark field: Treponema pallidum (syphilis, spirochetes). Giemsa: Rickettsia, Chlamydia (intracellular bacteria).

Obligate intracellular bacteria

Chlamydia, Rickettsia: obligate intracellular growth.

Binary fission

1 cell → 2 identical cells.

Intracellular growth

Hijack host cell (e.g., Chlamydia).

Conjugation

Plasmid transfer via sex pilus (F+ to F-).

Transduction

Bacteriophage transfers DNA.

Transformation

Uptake of naked DNA from environment.

Homologous recombination

Similar DNA sequences align and recombine.

Non-homologous recombination

No sequence similarity; enzymes mediate insertion.

Nutrients necessary for bacterial growth

Need: iron, carbon, nitrogen, etc. Siderophores steal iron from transferrin.

Types of bacteria based on oxygen requirements

Obligate aerobes, anaerobes, facultative, microaerophiles, aerotolerant anaerobes.

Bacterial growth curve phases

Lag: metabolic activity, no division. Log: exponential growth → antibiotics most effective. Stationary: growth = death. Death: decline in viable cells.

Prevention of iron acquisition by bacteria

Sequester iron via ferritin or reduce gut absorption.

Aerobes vs. anaerobes

Obligate aerobes: TB, Pseudomonas. Obligate anaerobes: Clostridium. Facultative: E. coli, Staph, Strep.

Detoxification by aerobic bacteria

Superoxide dismutase (SOD): detoxifies superoxide. Catalase & peroxidase: detoxify hydrogen peroxide.

Detoxifying enzymes in anaerobic bacteria

Obligate anaerobes lack SOD and catalase, hence oxygen is toxic to them.

Viral structures

Capsid (capsomers): protection & symmetry. Envelope: host-derived lipids + viral proteins. Tegument: enzymes/proteins (only in enveloped viruses). Genome: DNA or RNA.

Viral envelopes

Evade immune detection, use glycoprotein spikes to bind host receptors. More fragile → require direct contact for transmission.

Enveloped viruses

Heat/lipid-sensitive, transmitted via direct contact (blood, sex).

Non-enveloped viruses

Stable, transmitted via fecal-oral route, survive longer outside host.

Viral proteins

Surface proteins: serotypes, host receptor binding. Interior proteins: replication enzymes (polymerases, proteases).

Prions

Transmission: ingestion of contaminated tissue (e.g., brains). Inactivation: autoclaving, bleach, NaOH, phenol.

Atypical virus-like agents

Misfolded proteins → neural death, spongiform brains. No immune response; progressive and fatal. Ex: vCJD, Kuru, Scrapie, Mad Cow (BSE).

Viral infection

Viruses disrupt host function, kill cells via lysis or immune reaction. Cytopathic effects → symptoms, inflammation, tissue damage.

Viral growth curve

Eclipse: virus is replicating, not detectable. Rise: virus bursts out, symptoms begin.

Viral life cycle

Stages: Attachment → Entry → Uncoating → Replication → Assembly → Release. Enveloped: exit via budding (non-lethal). Non-enveloped: exit via lysis (kills host cell).

Antiviral treatment targets

Entry (fusion inhibitors), Uncoating inhibitors, Polymerase inhibitors, Protease inhibitors, Release inhibitors (e.g., neuraminidase inhibitors for flu).

Lysogenic cycle

Viral genome integrates → latent prophage. Reactivates later (e.g., herpes, HIV). Can encode toxins in bacteria → lysogenic conversion.

Lysogenic conversion

Prophage genes give bacteria new traits (e.g., toxin production → pathogenicity). Examples: Shiga toxin, botulinum toxin.

Latency

Latency: repressor proteins halt viral gene expression. Reactivation: triggered by UV, stress, etc. → active replication resumes.

Central dogma

DNA → mRNA → Protein. Viruses hijack host cell to replicate using this framework.

Viral replication sites

DNA viruses: nucleus. RNA viruses: cytoplasm (except retroviruses).

Viral genome replication methods

+ssRNA: directly translated; some also use RNA polymerase. -ssRNA, dsRNA: need viral RNA polymerase. Retroviruses: reverse transcriptase → DNA → integrated into host.

Antiviral therapy targets

Polymerases, proteases, entry/fusion inhibitors, release inhibitors are all drug targets.

Antigenic drift

Gradual mutation (e.g., seasonal flu).

Antigenic shift

Major reassortment (e.g., H1N1 pandemic). Common in influenza and other segmented RNA viruses.