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3.6 Axis Specification β Test 1
Q1. In C. elegans, the anteriorβposterior axis is set up when sperm entry causes:β Reorganization of the cytoskeleton and redistribution of PAR proteins
Q2. PAR proteins in C. elegans function to:β Establish and maintain cell polarity (anterior vs posterior)
Q3. P-granules in the C. elegans embryo are segregated to the:β Posterior germ-line precursor cell
Q4. The C. elegans embryo uses which modes of cell specification?β Both autonomous and conditional specification
Q5. When the AB and P1 blastomeres of C. elegans are separated, P1 forms all its normal cell types but AB does not. This shows that:β P1 is autonomously specified while AB needs cell interactions (conditional)
Q6. In C. elegans, the SKN-1 protein helps specify the:β EMS lineage (gut and mesoderm precursors)
Q7. In the sea urchin, beta-catenin accumulates predominantly in the:β Micromeres (vegetal pole), specifying endoderm and mesoderm
Q8. If GSK-3 is blocked in the sea urchin embryo, beta-catenin:β Accumulates in all blastula nuclei, so animal cells are specified as endoderm/mesoderm
Q9. When beta-catenin is prevented from entering the nucleus in the sea urchin, the embryo develops as:β A ciliated ectodermal ball (animalised)
Q10. In sea urchins, large micromeres act as a signalling centre by producing:β Paracrine and juxtacrine factors that specify neighbouring cell fates
Q11. Driesch's experiments separating early sea urchin blastomeres showed that each could form a:β Complete (but smaller) larva
Q12. Driesch's 'pressure-plate' experiment, which gave normal larvae after shuffling nuclei, showed that the prospective potency of a blastomere is:β Greater than its prospective fate
Q13. Driesch called the sea urchin embryo a 'harmonious equipotential system' because:β Its parts interact to form a single, normal embryo
Q14. In the sea urchin micromere gene network, Pmar1 acts by:β Repressing HesC (a repressor), thereby switching on skeletogenic genes
Q15. HesC in the sea urchin micromere network normally:β Represses genes that activate skeleton-forming programs
Q16. Injecting Pmar1 mRNA throughout a sea urchin embryo would cause:β All cells to take the skeletogenic fate and ingress into the blastocoel
Q17. The micromeres of the sea urchin are determined to become:β Skeletogenic mesenchyme that ingresses into the blastocoel
Q18. Transplanting micromeres to the animal pole of a host sea urchin embryo causes them to:β Ingress into the blastocoel and form ectopic skeletogenic mesenchyme