MCB 1 CELLS AND ORGANELLES Flashcards

Question

Which cytoskeletal element is the thickest? A. Actin filaments B. Intermediate filaments C. Microtubules D. Myosin E. Keratin

Answer 1

C The centrosome is the main microtubule organizing center (MTOC) in animal cells. Inside the centrosome, you usually find a pair of centrioles. Each centriole is a cylindrical structure made of microtubules arranged in a 9-triplet pattern (9 sets of triplet microtubules). These centrioles help organise microtubules during cell division (e.g., forming the spindle apparatus). 🧠 Key facts: Centrioles = inside the centrosome. Centrioles organize microtubules.

Answer 2

C rough ER Why? The nuclear envelope (double membrane around the nucleus) is directly continuous with the rough endoplasmic reticulum (RER). In fact, the outer membrane of the nuclear envelope is the rough ER — that's why ribosomes are found on its surface! Proteins made by these ribosomes can then easily enter the rough ER for further folding, modification, or transport. 🧠 Key point: Nuclear envelope outer membrane = continuous with rough ER membrane.

Answer 3

D peroxisomes Explanation: Zellweger syndrome is a peroxisomal biogenesis disorder. Patients lack functional peroxisomes, because the proteins needed to form them (peroxins) are defective. Peroxisomes are important for: Oxidising very long chain fatty acids Detoxifying hydrogen peroxide Without peroxisomes, toxic substances accumulate and cause major developmental issues, especially affecting the brain, liver, and kidneys. Why are the others wrong? A. Mitochondria → Present and functioning normally in Zellweger; it's peroxisomes that are missing. B. Ribosomes → Ribosomes are fine — they make proteins everywhere. C. Lysosomes → Lysosomes are fine — different organelles entirely. E. Smooth ER → Smooth ER still works — involved in lipid synthesis, detox, not affected in Zellweger. Memory Tip 🧠: "Zellweger = Zapped peroxisomes" 🧃 Summary: Zellweger = missing peroxisomes → accumulation of toxic lipids → serious disease.

Answer 4

37. B. Tubulin dimers ✅ And you are absolutely correct! Why? Microtubules are hollow cylindrical tubes made by polymerising tubulin dimers. Each dimer consists of one α-tubulin and one β-tubulin. These dimers stack head-to-tail into protofilaments, and 13 protofilaments come together side-by-side to form a complete microtubule. 🧠 Memory Tip: Microtubules = Micro-tube made of tubulin. (Micro-TUBules → TUBulin) Why the others are wrong: A. Actin → builds microfilaments (thinner than microtubules). C. Keratin → makes intermediate filaments (strength + support, not hollow tubes). D. Spectrin → connects cytoskeleton to membrane (especially in RBCs). E. Myosin → motor protein walking along actin, not structural.

Answer 5

✅ Answer = B. Kinesin Why? Kinesin is the motor protein that walks along microtubules toward the (+) end (usually toward the cell periphery). It uses ATP to "walk" — like tiny legs — carrying vesicles, organelles, and other cargo toward the outer edge of the cell. Meanwhile: Dynein moves cargo toward the (–) end → toward the nucleus (the cell centre). 🧠 Memory Tip: Kinesin Kicks outward (K = Kicks = away from centre). Dynein Drags inward (D = Drags = toward centre). Why the others are wrong: A. Dynein → moves inward, not outward. C. Actin → structural filament, not a motor protein itself. D. Spectrin → helps maintain cell shape, not a motor. E. Lamin → forms nuclear lamina (inside nucleus), no role in transport. 🌟 Summary: Kinesin = "Kick cargo out" along microtubules to cell periphery! Dynein = "Drag cargo in" toward the nucleus!

Answer 6

✅ Answer = B. Forms coated vesicles Why? Clathrin is a protein that forms a special "coated pit" on the inside of the plasma membrane. It helps form vesicles during endocytosis (bringing substances into the cell) and sometimes in Golgi transport too. It coats the vesicle like a cage, helping it bud off from the membrane. 🧠 Memory Tip: "Clathrin coats vesicles like a clamshell" 🐚 Why the others are wrong: A. Organises chromatin → That's histone proteins' job, not clathrin. C. Stabilises actin filaments → That’s actin-binding proteins, not clathrin. D. Synthesises phospholipids → That happens in the smooth ER. E. Forms microtubules → Tubulin forms microtubules, not clathrin. 🌟 Summary: Clathrin = vesicle coat protein, essential for endocytosis and vesicle trafficking!

Answer 7

✅ Answer = B. Basal body Why? Cilia (those hair-like projections on cells) are anchored into the plasma membrane by a basal body. The basal body is structurally very similar to a centriole (made of microtubule triplets in a 9+0 arrangement). It acts like a foundation, holding the cilium steady while the microtubules inside the cilium allow it to move (beating back and forth). Why the others are wrong: A. Centrosome → Organises microtubules inside the cell, not directly linked to cilia anchoring. C. Ribosome → Protein synthesis, nothing to do with cilia. D. Peroxisome → Metabolises lipids and toxins, not related to cilia. E. Nucleolus → Ribosome assembly, inside the nucleus! 🧠 Memory Tip: Basal Body = Base for Beating cilia! 🌀 🌟 Summary: Cilia are rooted into the membrane using a basal body, much like a tree rooted into the ground!

Answer 8

A ✅ Correct answer: A. Taxol Explanation: Taxol (also called Paclitaxel) prevents microtubule disassembly by stabilising microtubules. It freezes the microtubules in place, preventing them from shortening (disassembly). This blocks mitosis (cell division), which is why Taxol is used as an anti-cancer drug (stops cancer cells from dividing). Colchicine, on the other hand, prevents microtubule assembly (not disassembly). It binds free tubulin and prevents new microtubules forming. Used in diseases like gout (inflammatory disease). 🧠 Memory Tip: Taxol "Tacks" microtubules in place = prevents disassembly! Colchicine "Clogs" tubulin = prevents assembly! 🔵 Summary: Taxol = stops disassembly ✅ Colchicine = stops assembly ❌

Answer 9

Gelosin The 'gel to sol' transition means changing the cytoplasm from a stiff gel-like state to a more fluid (sol) state. Gelsolin is the protein that severs actin filaments and caps the plus (+) ends, preventing re-polymerisation. When actin is cut into small fragments, the network becomes less rigid and more fluid — that’s the "gel to sol" transition! 🧠 Memory Tip: Gelsolin = Gel-softener! ("Sol" in gelsolin = sol = fluid)

Answer 10

Structural support Why? Intermediate filaments (IFs) are very strong, rope-like fibers. Their main role is to give mechanical strength to cells — they protect cells from mechanical stress (like stretching or pressure). Found especially in cells exposed to stress: Keratin in skin Neurofilaments in neurons Lamins inside the nucleus (support the nuclear envelope) 🧠 Memory Tip: Intermediate filaments = Inner Frame (support frame of the cell)! 🛡️ Why the others are wrong: A. Active movement → Microfilaments (actin) and microtubules are for movement. C. Vesicle transport → Done by microtubules + motor proteins (kinesin, dynein). D. Signal transmission → Often by proteins and receptors, not intermediate filaments. E. Protein translation → Done by ribosomes. 🌟 Summary: Intermediate filaments = strong, stable support system, protecting cells against mechanical damage.

Answer 11

C. Rough ER N-linked glycosylation is the attachment of sugar chains to the nitrogen atom (N) on an asparagine residue of a protein. This process starts in the rough ER, not in the cytosol. A pre-assembled oligosaccharide (a sugar tree) is attached to proteins inside the ER lumen while the protein is being synthesised. After initial attachment in the ER, the sugars can be further modified in the Golgi apparatus. 🧠 Memory Tip: N-linked starts in the N-ER (N for N-linked, N for rough ER)! (Also think rough ER = ribosomes = secretory proteins = N-glycosylation.) - N-linked glycosylation starts in the rough ER. - O-linked glycosylation mostly happens in the Golgi.

Answer 12

C. Inclusion cell disease Why? Inclusion cell disease (I-cell disease) is a lysosomal storage disorder caused by defective lysosomal enzyme targeting. The defective enzyme targeting leads to enzymes being sent to the wrong part of the cell (they don’t reach the lysosomes). As a result, undigested substrates accumulate in the lysosomes, forming "inclusions" in the cells. I-cell disease results in severe developmental delays, organ dysfunction, and other issues due to the accumulation of waste inside the cells. I-cell disease = "I" for "incorrect enzyme targeting" to lysosomes. 🌟 Summary: Inclusion cell disease (I-cell disease) = defect in lysosomal enzyme targeting, causing accumulation of waste in cells.

MCB 1 CELLS AND ORGANELLES Flashcards

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