Explain why many developmental genes encode either transcription factors or signaling molecules.

Bird beaks develop from an embryonic group of cells called neural crest cells that are part of the neural tube, which gives rise to the spinal column and related structures. Amazingly, neural crest cells can be surgically transplanted from one embryo to another, even between embryos of different species. When quail neural crest cells were transplanted into duck embryos, the beak of the host embryo developed into a shape similar to that found in quails, creating the 'quck.' Duck cells were recruited in addition to the quail cells to form part of the quck beak. Conversely, when duck neural crest cells were transplanted into quail embryos, the beak of the embryo resembled that of a duck, creating a 'duail,' and quail cells were recruited to form part of the beak. What do these experiments tell you about the autonomy or nonautonomy of the transplanted and host cells during beak development?

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.

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

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?

Consider the even-skipped regulatory sequences in the following figure:

How are the sharp boundaries of expression of Eve Stripe 2 formed?

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.

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?

What is the difference between a parasegment and a segment in Drosophila development? Why do developmental biologists think of parasegments as the subdivisions that are produced during the development of flies?

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?

Compare and contrast the specification of segmental identity in Drosophila with that of floral organ specification in Arabidopsis. What is the same in this process, and what is different?

Actinomycin D is a drug that inhibits the activity of RNA polymerase II. In the presence of actinomycin D, early development in many vertebrate species, such as frogs, can proceed past the formation of a blastula, a hollow ball of cells that forms after early cleavage divisions, but development ceases before gastrulation (the stage at which cell layers are established). What does this tell you about maternal versus zygotic gene activity in early frog development?

Ablation of the anchor cell in wild-type C. elegans results in a vulva-less phenotype.

What phenotype is to be expected if the anchor cell is ablated in a let-23 loss-of-function mutant?

Ablation of the anchor cell in wild-type C. elegans results in a vulva-less phenotype.

What about if the anchor cell is ablated in a let-23 gain-of-function mutant?

In gain-of-function let-23 and let-60 C. elegans mutants, all of the vulval precursor cells differentiate with 1° or 2° fates. Do you expect adjacent cells to differentiate with 1° fates or with 2° fates? Explain.

In mammals, identical twins arise when an embryo derived from a single fertilized egg splits into two independent embryos, producing two genetically identical individuals.

What limits might there be, from a developmental genetic viewpoint, as to when this can occur?

In mammals, identical twins arise when an embryo derived from a single fertilized egg splits into two independent embryos, producing two genetically identical individuals.

The converse phenotype, fusion of two genetically distinct embryos into a single individual, is also known. What are the genetic implications of such an event?

The bicoid gene is a coordinate maternal-effect gene.

A female Drosophila heterozygous for a loss-of-function bicoid allele is mated to a male that is heterozygous for the same allele. What are the phenotypes of their progeny?

The bicoid gene is a coordinate maternal–effect gene. A female that is homozygous for a loss-of-function bicoid allele is mated to a wild-type male. What are the phenotypes of their progeny?

The bicoid gene is a coordinate maternal–effect gene. If loss of bicoid function in the egg leads to lethality during embryogenesis, how are females homozygous for bicoid produced? What is the phenotype of a male homozygous for bicoid loss-of-function alleles?

Given that maternal Bicoid activates the expression of hunchback, what would be the consequence of adding extra copies of the bicoid gene by transgenic means to a wild-type female with two copies, thus creating a female fly with three or four copies of the bicoid gene? How would the hunchback expression be altered? What about the expression of other gap genes and pair-rule genes?

The pair-rule gene fushi tarazu is expressed in the seven even-numbered parasegments during Drosophila embryogenesis. In contrast, the segment polarity gene engrailed is expressed in the anterior part of each of the 14 parasegments. Since both genes are active at similar times and places during development, it is possible that the expression of one gene is required for the expression of the other. This can be tested by examining expression of the genes in a mutant background—for example, looking at fushi tarazu expression in an engrailed mutant background, and vice versa. Given the hierarchy of gene action during Drosophila embryogenesis, what might you predict to be the result of these experiments?

The pair-rule gene fushi tarazu is expressed in the seven even-numbered parasegments during Drosophila embryogenesis. In contrast, the segment polarity gene engrailed is expressed in the anterior part of each of the 14 parasegments. Since both genes are active at similar times and places during development, it is possible that the expression of one gene is required for the expression of the other. This can be tested by examining the expression of the genes in a mutant background—for example, looking at fushi tarazu expression in an engrailed mutant background, and vice versa. Based on your prediction, can you predict the phenotype of the fushi tarazu and engrailed double mutant?

In contrast to Drosophila, some insects (e.g., centipedes) have legs on almost every segment posterior to the head. Based on your knowledge of Drosophila, propose a genetic explanation for this phenotype, and describe the expected expression patterns of genes of the Antennapedia and bithorax complexes.

You are traveling in the Netherlands and overhear a tulip breeder describe a puzzling event. Tulips normally have two outer whorls of brightly colored petal-like organs, a third whorl of stamens, and an inner (fourth) whorl of carpels. However, the breeder found a recessive mutant in his field in which the outer two whorls were green and sepal-like, whereas the third and fourth whorls both contained carpels. What can you speculate about the nature of the gene that was mutated?

A powerful approach to identifying genes of a developmental pathway is to screen for mutations that suppress or enhance the phenotype of interest. This approach was undertaken to elucidate the genetic pathway controlling C. elegans vulval development. A lin-3 loss-of-function mutant with a vulva-less phenotype was mutagenized. Based on your knowledge of the genetic pathway, what types of mutations will suppress the vulva-less phenotype?

A powerful approach to identifying genes of a developmental pathway is to screen for mutations that suppress or enhance the phenotype of interest. This approach was undertaken to elucidate the genetic pathway controlling C. elegans vulval development. In a complementary experiment, a gain-of-function let-23 mutant with a multi-vulva phenotype was also mutagenized. What types of mutations will suppress the multi-vulva phenotype?

The Hoxd9–13 genes are thought to specify digit identity. What would be the consequence of ectopically expressing Hoxd10 throughout the developing mouse limb bud? What about Hoxd11? What about both Hoxd10 and Hoxd11?