set 4 Flashcards

(62 cards)

1
Q

4.1 – State the main difference between prokaryotes and eukaryotes.

A

Prokaryotes lack a membrane‑bound nucleus; eukaryotes possess a membrane‑bound nucleus.

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2
Q

4.1 – List the 3 domains in the current classification.

A

Bacteria, Archaea, Eukarya.

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3
Q

4.1 – What methods are used today to infer evolutionary relationships?

A

Molecular sequence comparisons (e.g., rRNA genes, whole‑genome DNA), phylogenomics, and comparative genomics.

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4
Q

4.1 – What is the Candidate Phyla Radiation (CPR)?

A

A large set of bacterial lineages discovered by environmental DNA sequencing; many are unculturable and very small (~400 nm).

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5
Q

4.1 – Define extremophiles and give 3 archaeal examples.

A

Organisms thriving in extreme conditions. Examples: methanogens (H₂ + CO₂ → CH₄), halophiles (high salt), thermacidophiles (hot + acidic).

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6
Q

4.1 – Why are Archaea considered more similar to Eukaryotes than to Bacteria?

A

Core information‑processing machinery (DNA replication, transcription, RNA processing, translation initiation) resembles eukaryotic systems.

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7
Q

4.1 – Typical sizes of bacteria/archaea vs plant/animal cells?

A

Bacteria/Archaea: 1–5 μm; Plant/Animal: 10–100 μm.

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8
Q

4.2 – List the three limits on cell size.

A

1) Surface area:volume (SA:V) constraints, 2) Diffusion rates of molecules, 3) Need to maintain adequate local concentrations of reactants/enzymes.

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9
Q

4.2 – Explain why SA:V declines as a cell grows.

A

Volume scales with length³; surface area with length² → larger cells have proportionally less surface area for exchange.

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10
Q

4.2 – Give a biological example of maximizing SA:V.

A

Intestinal microvilli—fingerlike projections that greatly increase surface area for absorption.

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11
Q

4.2 – Define diffusion.

A

Passive movement of molecules from high → low concentration due to random thermal motion.

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12
Q

4.2 – How do cells overcome slow diffusion of large molecules?

A

Use carrier proteins, active transport, and cytoplasmic streaming to move materials.

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13
Q

4.2 – Why are many small cells better than one large cell?

A

Collectively they have greater total SA, shorter diffusion distances, and can specialize.

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14
Q

4.2 – What happens to collision frequency of enzymes/substrates as cell size increases at constant concentrations?

A

It drops; fewer productive collisions per time → reactions slow unless compartmentalized or concentrations increase.

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15
Q

4.3 – How does compartmentalization speed metabolism?

A

By localizing enzymes + substrates (e.g., Krebs cycle enzymes in mitochondria), raising effective concentrations and collision rates.

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16
Q

4.3 – Define organelle.

A

A membrane‑bound compartment in eukaryotic cells with specialized functions.

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17
Q

4.4 – Define nuclear envelope and nucleolus.

A

Nuclear envelope: double membrane surrounding nucleus. Nucleolus: site of rRNA synthesis and ribosomal subunit assembly.

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18
Q

4.4 – Where is DNA found in Bacteria/Archaea vs Eukaryotes, and what is its shape?

A

Bacteria/Archaea: nucleoid, circular DNA (histone‑like proteins in Archaea). Eukaryotes: nucleus, linear DNA bound to histones.

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19
Q

4.4 – What R‑groups make histones bind DNA?

A

Basic/positively charged residues (Lys, Arg) bind the negatively charged DNA backbone.

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20
Q

4.4 – List three cytoskeletal systems and a general role.

A

Microtubules, microfilaments, intermediate filamentsstructure, motility, intracellular transport.

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21
Q

4.4 – Define exocytosis and endocytosis.

A

Exocytosis: vesicles fuse with plasma membrane to export contents. Endocytosis: plasma membrane invaginates to import extracellular material.

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22
Q

4.4 – How do cells take up cholesterol via endocytosis?

A

Receptor‑mediated endocytosis: LDL receptors bind LDL‑cholesterol, clathrin‑coated pits internalize → endosome → lysosome to release cholesterol.

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23
Q

4.4 – Define binary fission.

A

Asexual division of prokaryotes: DNA replicates and the cell splits, yielding genetically identical cells.

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24
Q

4.4 – Two reasons meiosis generates genetic diversity.

A

Independent assortment of chromosomes and homologous recombination (crossing over).

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25
4.4 – Explain **operons** vs eukaryotic gene expression.
**Bacteria** often transcribe **polycistronic mRNA** (operons) encoding **several proteins**; **eukaryotes** typically produce **monocistronic mRNAs**.
26
4.5 – Main function of **mitochondria** (don’t say powerhouse!)
**Aerobic respiration**: oxidize fuels and capture energy in **ATP** via **TCA cycle** and **oxidative phosphorylation**.
27
4.5 – Define **cristae** and **matrix**.
**Cristae**: folds of the **inner mitochondrial membrane** housing ETC complexes. **Matrix**: internal **aqueous** compartment with **TCA enzymes**.
28
4.5 – How do **number/location** of mitochondria vary with cell type?
Cells with **high ATP demand** have **many mitochondria** positioned near **energy‑using sites** (e.g., **sperm tail**, **muscle fibrils**).
29
4.5 – Key facts about **mtDNA**.
**Circular**, ~**16.5 kb**, encodes **37 genes** (incl. **tRNAs**); many mitochondrial disorders involve **tRNA gene** mutations; **maternal inheritance**.
30
4.5 – Why are **mitochondrial diseases** maternally inherited?
**Zygote cytoplasm** (and mitochondria) comes predominantly from the **oocyte**; sperm mitochondria are **not typically transmitted**.
31
4.5 – Why would mutant **mitochondrial tRNAs** impair function?
Faulty **tRNAs** **block mitochondrial translation**, reducing **ETC/TCA proteins** → **ATP deficiency**.
32
4.5 – Briefly explain the symptoms in **MELAS**: muscle weakness, lactic acidosis, stroke‑like episodes.
**ATP deficit** in muscle → **weakness**; impaired oxidative phosphorylation → ↑**glycolysis** → **lactate** (**acidosis**); **neuronal energy failure** → **stroke‑like** episodes.
33
4.5 – Main functions and compartments of the **chloroplast**.
**Photosynthesis**; **thylakoid** membranes (light reactions), **grana** stacks; **stroma** (CO₂ fixation).
34
4.5 – Name the cycle that reduces **CO₂ to sugar** in chloroplasts.
**Calvin cycle** (occurs in the **stroma**).
35
4.5 – Why do chloroplasts carry **ribosomes and circular DNA**?
They encode/translate **some of their own proteins**, supporting an **endosymbiotic origin**.
36
4.5 – How are **nitrates** formed in soil from **N₂** and why do chloroplasts reduce nitrate?
**Nitrogen‑fixing bacteria** convert **N₂ → NH₃/NH₄⁺**, and **nitrifying bacteria** oxidize to **NO₂⁻/NO₃⁻** (also via lightning/industrial). Chloroplasts reduce **NO₃⁻ → NH₃/NH₄⁺** for **amino acid** synthesis.
37
4.5 – Why are **NH₃/NH₄⁺** essential for protein synthesis?
They provide the **amino group** incorporated into **amino acids**.
38
4.6 – Summarize the **endosymbiont theory**.
**Mitochondria** and **chloroplasts** originated when ancestral **prokaryotes** were **engulfed** by a proto‑eukaryote and became **symbionts**.
39
4.6 – Give **two arguments FOR** endosymbiosis.
**Circular genomes**, **bacterial‑sized ribosomes**, **binary‑fission‑like division**, **double membranes** resembling engulfment.
40
4.6 – Give **one argument AGAINST** or caveat.
Modern organelles depend on **nuclear‑encoded proteins** and cannot **live independently**; genomes are **highly reduced**.
41
4.6 – Define **aerobic heterotrophic** vs **photosynthetic autotrophic** prokaryote.
**Aerobic heterotroph**: uses **O₂** and **organic carbon**; source of **mitochondrion**. **Photosynthetic autotroph**: uses **light** to fix **CO₂**; source of **chloroplast**.
42
4.7 – List the **endomembrane system** components.
**Nuclear envelope, ER (rough + smooth), Golgi apparatus, lysosomes, vesicles**, and the **plasma membrane** (functionally connected).
43
4.7 – General function of **rough ER** vs **smooth ER**.
**Rough ER**: **synthesizes** membrane/secretory proteins. **Smooth ER**: **lipid/steroid synthesis**, **detoxification** (enzymes on cytosolic face).
44
4.7 – General function of the **Golgi apparatus**.
**Modifies, sorts, and packages** proteins/lipids (e.g., adds **polysaccharides** to proteins) for delivery to **lysosomes, plasma membrane, secretion**.
45
4.7 – What are **secretory vesicles**?
Vesicles that **bud from Golgi**, move to the **plasma membrane**, and **fuse** to release cargo (**exocytosis**).
46
4.7 – Define **lysosome** and **hydrolases**.
**Lysosome**: acidic organelle containing **hydrolases** that degrade **all biomacromolecules**; inner membrane is **carbohydrate‑coated** for protection.
47
4.7 – Why can hydrolases digest **any macromolecule**?
Because the set includes **proteases**, **nucleases**, **lipases**, **glycosidases**, **phosphatases**, etc., targeting **peptide, glycosidic, phosphodiester, ester** bonds.
48
4.7 – Explain **I‑cell disease** and **mannose‑6‑phosphate (M6P)**.
A defect in the **GlcNAc‑phosphotransferase** that generates **M6P** tags → enzymes **aren’t targeted** to lysosomes and are **secreted** instead; cells show **inclusion bodies**.
49
4.7 – Why are lysosomal enzymes **secreted** when they **lack M6P**?
Without **M6P**, they **don’t bind the M6P receptor** in Golgi and **follow the default secretory pathway** to the cell surface.
50
4.8 – General function of **peroxisomes**.
**Oxidize** fatty acids and other substrates; generate **H₂O₂** and degrade it via **catalase/peroxidases**.
51
4.8 – How do peroxisomes remove **H₂O₂**?
**Catalase** converts **2 H₂O₂ → 2 H₂O + O₂** (or uses H₂O₂ to **oxidize** other substrates).
52
4.8 – Explain **X‑linked adrenoleukodystrophy (ALD)** biochemically.
**Defective peroxisomal β‑oxidation** of **very‑long‑chain fatty acids (VLCFAs, e.g., C26:0)** → accumulation damages **myelin**.
53
4.8 – Why does **C26:0** accumulation damage **myelin**?
VLCFAs **disrupt membrane lipids** and **myelin stability**, triggering **inflammation** and **degeneration** of myelin sheaths.
54
4.8 – How does **Lorenzo’s Oil** help ALD?
A **4:1 mix of C18:1:C22:1** **competitively inhibits FA elongation**, lowering **C26:0** synthesis → reduces VLCFA accumulation.
55
4.8 – General functions of **vacuoles** in animals/yeast.
**Storage** and **transport**; **phagocytosis** forms a **phagosome** that fuses with lysosomes for digestion.
56
4.8 – Role of the **central vacuole** in plants.
Maintains **turgor pressure** to keep tissues rigid; loss of pressure → **wilting**.
57
4.8 – Define **phagocytosis** and **phagosome**.
**Phagocytosis**: uptake of large particles by membrane **engulfment**; **phagosome**: the internal **vesicle** formed.
58
4.9 – What are **ribosomes** and are they membrane‑bound?
**Ribonucleoprotein complexes** (rRNA + proteins) that **synthesize proteins**; **not** membrane‑bound.
59
4.9 – Explain **Svedberg (S)** units and why subunits don’t add up arithmetically.
**S** measures **sedimentation rate** (size/shape dependent). Combined particles **sediment differently**, so **S values aren’t additive**.
60
4.9 – Contrast **eukaryotic** and **prokaryotic** ribosome **S values**.
**Eukaryote**: **80S** (60S + 40S). **Bacteria/Archaea**: **70S** (50S + 30S).
61
SG – Compute **SA, V, SA:V** for cubes conceptually and explain significance.
**SA = 6ℓ²**, **V = ℓ³**, **SA:V = 6/ℓ** → as **ℓ increases**, **SA:V** decreases, limiting **exchange** and **metabolic rate** per volume.
62
SG – Name **membrane‑bound** organelles covered in this set.
**Nucleus**, **ER**, **Golgi**, **lysosomes**, **peroxisomes**, **vacuoles**, **mitochondria**, **chloroplasts** (plants/algae).