During wing development in chick, if Apical Ectodermal Ridge (AER) is removed, the limb development ceases, on the other hand placing leg mesenchyme directly beneath the wing AER, distal hindlimb structures develop at the end of the wing, and if limb mesenchyme is replaced by non-limb mesenchyme beneath AER, the AER regresses. This may demonstrate that: A. the limb mesenchyme cells induce and sustain AER. B. the mesenchyme cells specify the type: wing or limb. C. the AER is responsible for specifying the type: wing or limb. D. the AER is responsible for sustained outgrowth and development of the limb. E. the AER does not specify the type: wing or limb. Which combination of above statements is demonstrated by the experiment?
A, B, D and E only
Chick Wing Development Experiments
This question describes a series of classic experiments conducted during chick limb development. These experiments help us understand the roles of two key components: the Apical Ectodermal Ridge (AER) and the underlying mesenchyme cells.
Understanding the Experiments
Let's break down each experiment and its result:
- If the Apical Ectodermal Ridge (AER) is removed during wing development, the limb development stops (ceases).
- If leg mesenchyme is placed directly under the wing AER, structures typical of the distal hindlimb (leg) develop at the end of the wing.
- If the limb mesenchyme under the AER is replaced by non-limb mesenchyme, the AER disappears (regresses).
Analyzing the Statements
Now let's see which of the given statements are supported by these experimental outcomes:
- Statement A: "the limb mesenchyme cells induce and sustain AER."
Experiment 3 shows that replacing limb mesenchyme with non-limb mesenchyme causes the AER to regress. This strongly suggests that limb mesenchyme is necessary to keep the AER healthy and functional (sustain it). While 'induce' isn't directly tested here (as AER is already present), its dependence on limb mesenchyme for survival is clear. This statement is supported. - Statement B: "the mesenchyme cells specify the type: wing or limb."
Experiment 2 is critical here. When leg mesenchyme is placed under wing AER, the resulting structures are from the leg (hindlimb), not the wing. This shows that the mesenchyme determines whether a wing or leg develops, overriding the 'identity' of the AER. This statement is supported. - Statement C: "the AER is responsible for specifying the type: wing or limb."
Experiment 2 directly contradicts this. If the AER specified the type, then a wing AER should lead to a wing structure, regardless of the mesenchyme. But the result was a leg structure. This statement is not supported. - Statement D: "the AER is responsible for sustained outgrowth and development of the limb."
Experiment 1 shows that removing the AER stops limb development. This demonstrates that the presence of the AER is essential for the limb to continue growing and developing properly. This statement is supported. - Statement E: "the AER does not specify the type: wing or limb."
This statement is the opposite of statement C. As shown by Experiment 2, the AER from a wing did not cause wing development when paired with leg mesenchyme; leg structures developed. This confirms that the AER does not determine whether the limb becomes a wing or a leg. This statement is supported.
Conclusion
Based on the analysis of the experiments, the statements supported are A, B, D, and E.
Statement C is explicitly disproven by the experiments.
Therefore, the combination of statements demonstrated by the experiments is A, B, D and E.
Important Questions from Morphogenesis and organogenesis in animals
A "morphogen" can determine the fate of a cell by its concentration. Given below are some statements on the experiment performed to study the gradient-dependent effect of the morphogen, activin on cell fate by placing activin (4 nm)-secreting beads on unspecified cells from an early Xenopus embryo:
A. Beads without activin did not elicit expression of either Xbra or goosecoid genes.
B. Cells nearest to the beads getting highest concentration of activin induced goosecoid gene whose product is a transcription factor, specifies the frog's dorsal-most structures.
C. Cells nearest to the beads getting highest concentration of activin induced Xbra gene whose product is a transcription factor, specifies the frog's dorsal-most structures.
D. Cells farthest from the beads getting negligible activin activate Xbra gene and become blood vessels and heart.
E. Cells farthest from the beads getting negligible activin, activated neither Xbra nor goosecoid and the 'default' gene expression instructed the cells to become blood vessels and heart.
Which of the above observations and conclusions drawn are correct?
The individuals considered in this question are having two haploid sets of autosomes and no Y- chromosome. The X∶A ratio of the individuals, the type of organisms chosen, their primary sex and number of Barr bodies expected in their cells are shown in the table below:
X∶A ratio Organism Primary Sex Number of Barr bodies i. 0.5
ii. 2
A. Human
B. Drosophila
I. Male
II. Female
III. Metafemale
a. Zero
b. One
c. Two
d. Three
Select the option below with all correct matches:
Several marine organism release their gametes into the environment, where sperm attraction and subsequent events lead to successful fertilization. With reference to sea urchins, which one of the following statements is NOT true?
The following statements regarding the generation of dorsal/ventral axis in Drosophila was made:
A. Gurken protein moves along with the oocyte nucleus and signals follicle cells to adopt the ventral fate.
B. Maternal deficiencies of either the gurken or torpedo gene cause ventralization of the embryo.
C. Gurken is active only in the oocyte and Torpedo is active only in the somatic follicle cells.
D. The Pipe protein is made in the dorsal follicle cells.
E. The highest concentration of Dorsal is in the dorsal cell nuclei, which becomes the mesoderm.
Which one of the following combination of the above statements is true?
Human polysyndactyly (joining of extra digits) syndrome results from a homozygous mutation at
