14. Genetic Control of Development

Which of the following HOX clusters are responsible for forming the abdominal in Drosophila development?

In Arabidopsis, which class of HOX genes are responsible for forming the plant carpels?

In this chapter, we have focused on large-scale as well as the inter- and intracellular events that take place during embryogenesis and the formation of adult structures. In particular, we discussed how the adult body plan is laid down by a cascade of gene expression, and the role of cell–cell communication in development. Based on your knowledge of these topics, answer several fundamental questions:

How do we know that eye formation in all animals is controlled by a binary switch gene?

How is positional information provided along the anterior–posterior axis in Drosophila? What are the functions of bicoid and nanos?

Early development in Drosophila is atypical in that pattern formation takes place in a syncytial blastoderm, allowing free diffusion of transcription factors between nuclei. In many other animal species, the fertilized egg is divided by cellular cleavages into a larger and larger number of smaller and smaller cells.

How must the model that describes Drosophila development be modified for describing animal species whose early development is not syncytial?

Early development in Drosophila is atypical in that pattern formation takes place in a syncytial blastoderm, allowing free diffusion of transcription factors between nuclei. In many other animal species, the fertilized egg is divided by cellular cleavages into a larger and larger number of smaller and smaller cells.

What constraints does the formation of a syncytial blastoderm impose on the mechanisms of pattern formation?

Consider the even-skipped regulatory sequences in Figure 18.9.

Explain what you expect to see happen to even-skipped stripe 2 if it is expressed in a Krüppel mutant background. What about a hunchback mutant background? A giant mutant background? A bicoid mutant background?

Consider the even-skipped regulatory sequences in Figure 18.9.

Consider the binding sites for gap proteins and Bicoid in the stripe 2 enhancer module. What sites are occupied in parasegments 2, 3, and 4, and how does this result in expression or no expression?

Consider the even-skipped regulatory sequences in Figure 18.9.

How are the sharp boundaries of expression of eve stripe 2 formed?

What is the phenotype of maternal-effect mutations?

What aspects of development do maternal-effect genes control?

When are gene products from these genes made, and where are they located?

What are maternal-effect genes?

Why do loss-of-function mutations in Hox genes usually result in embryo lethality, whereas gain-of-function mutants can be viable? Why are flies homozygous for the recessive loss-of-function alleles  and  viable?

What is the phenotype associated with zygotic gene mutations?