Drosophila eye morphology: The classic Bar eye phenotype in Drosophila melanogaster is primarily caused by which chromosomal change?
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ADuplication in region 16A of the X chromosome
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BDeletion in region 16A of the X chromosome
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CPresence of an extra X chromosome (XXY) alone
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DA single base substitution at the eye-color locus
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ETranslocation between X and autosome 2
Answer
Correct Answer: Duplication in region 16A of the X chromosome
Explanation
Introduction / Context:The Bar eye phenotype (narrow, slit-like eyes) is a classic example used to illustrate gene dosage and chromosomal rearrangements in fruit flies. Understanding its cytogenetic basis helps connect phenotype to specific structural variations.
Given Data / Assumptions:
- Phenotype: Bar (reduced eye size, slit-like appearance).
- Chromosomal region implicated: X chromosome, cytological band around 16A.
- Mechanism: copy number change (dosage effect).
Concept / Approach:Bar results from a tandem duplication in the 16A region on the X chromosome. Increased gene dosage in this region reduces eye size. Further duplication (double Bar) exacerbates the phenotype, demonstrating dosage sensitivity rather than a simple point mutation or aneuploidy per se.
Step-by-Step Solution:
Identify the phenotype and associated locus (X, 16A).Recall that Bar is due to tandem duplication, not deletion.Understand dosage: more copies intensify Bar phenotype.Select “Duplication in region 16A of the X chromosome”.Verification / Alternative check:Classical cytogenetic studies and genetic mapping confirm increased copy number at 16A correlates with Bar and double Bar phenotypes.
Why Other Options Are Wrong:
- Deletion: would typically reduce dosage; does not explain Bar.
- Extra X (XXY): affects sex determination and viability but is not the primary cause of Bar.
- Point mutation or translocation: not the canonical mechanism for Bar.
Common Pitfalls:Confusing Bar (dosage/duplication) with white or sepia (point mutations) eye-color phenotypes controlled by single genes.
Final Answer:Duplication in region 16A of the X chromosome