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Ch. 23 - Developmental Genetics

Chapter 22, Problem 13

The Drosophila homeotic mutation spineless aristapedia (ssᵃ) results in the formation of a miniature tarsal structure (normally part of the leg) on the end of the antenna. What insight is provided by (ssᵃ) concerning the role of genes during determination?

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Everyone. Let's take a look at this question together. What is the normal structure on which the miniature tar cell structure is formed due to the S S A mutation? So this miniature tar cell structure, we know tar cell means that it is normally found on the legs of insects. But when we have this S S A mutation, which the S S A mutation is the spineless a recipe. A mutation. It is a home idiotic mutation which causes the formation of the miniature parcel structure to form on the and of the antenna of the insect instead of being formed on the legs due to that mutation. So answer choice C is the correct answer because we know that the tar cell structure is normally found on the legs of the insects and are used for walking and gripping surfaces. But in the case of this S a mutation or the spineless Arisa PD A mutation, it results in the formation of that miniature tar cell structure on the end of the antenna of the insect. So answer choice C is the correct answer. I hope you found this video to be helpful. Thank you and goodbye.
Related Practice
Textbook Question
How can you determine whether a particular gene is being transcribed in different cell types?
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Textbook Question

You observe that a particular gene is being transcribed during development. How can you tell whether the expression of this gene is under transcriptional or translational control?

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Textbook Question

The homeotic mutation Antennapedia causes mutant Drosophila to have legs in place of antennae and is a dominant gain-of-function mutation. What are the properties of such mutations? How does the Antennapedia gene change antennae into legs?

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Textbook Question

Embryogenesis and oncogenesis (generation of cancer) share a number of features including cell proliferation, apoptosis, cell migration and invasion, formation of new blood vessels, and differential gene activity. Embryonic cells are relatively undifferentiated, and cancer cells appear to be undifferentiated or dedifferentiated. Homeotic gene expression directs early development, and mutant expression leads to loss of the differentiated state or an alternative cell identity. M. T. Lewis [(2000). Breast Can. Res. 2:158–169] suggested that breast cancer may be caused by the altered expression of homeotic genes. When he examined 11 such genes in cancers, 8 were underexpressed while 3 were overexpressed compared with controls. Given what you know about homeotic genes, could they be involved in oncogenesis?

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Textbook Question

The specification of the anterior–posterior axis in Drosophila embryos is initially controlled by various gene products that are synthesized and stored in the mature egg following oogenesis. Mutations in these genes result in abnormalities of the axis during embryogenesis. These mutations illustrate maternal effect. How do such mutations vary from those produced by organelle heredity? Devise a set of parallel crosses and expected outcomes involving mutant genes that contrast maternal effect and organelle heredity.

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Textbook Question
Early development depends on the temporal and spatial interplay between maternally supplied material and mRNA and the onset of zygotic gene expression. Maternally encoded mRNAs must be produced, positioned, and degraded [Surdej and Jacobs-Lorena (1998). Mol. Cell Biol. 18:2892–2900]. For example, transcription of the bicoid gene that determines anterior–posterior polarity in Drosophila is maternal. The mRNA is synthesized in the ovary by nurse cells and then transported to the oocyte, where it localizes to the anterior ends of oocytes. After egg deposition, bicoid mRNA is translated and unstable bicoid protein forms a decreasing concentration gradient from the anterior end of the embryo. At the start of gastrulation, bicoid mRNA has been degraded. Consider two models to explain the degradation of bicoid mRNA: (1) degradation may result from signals within the mRNA (intrinsic model), or (2) degradation may result from the mRNA's position within the egg (extrinsic model). Experimentally, how could one distinguish between these two models?
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