What are the three germ layers formed during gastrulation, and what are the principal

In the early cleavage stages, when the embryo cannot yet feed, the developmental program is driven and controlled entirely by the material deposited in the egg by the mother.

Because of the many later developmental transformations that produce the elaborately structured organs, the body plan set up during gastrulation bears little resemblance to the body plan in the adult.

As development progresses, individual cells become more and more restricted in the range of cell types they can give rise to.

At different stages of embryonic development, the same signals are used over and over again by different cells, but with different biological outcomes.

Changes in the coding regions of genes involved in development are primarily responsible for the differences between species.

The cell cycle is the ticking clock that sets the tempo of developmental processes, with maturational changes in gene expression being dependent on cell-cycle progression.

Name the four processes that are fundamental to animal development, and describe each of them in a single sentence.

What are the three germ layers formed during gastrulation, and what are the principal structures each gives rise to in the adult?

In the early Drosophila embryo, there seems to be no requirement for the usual forms of cellcell signaling; instead, transcriptional regulators and mRNA molecules move freely between nuclei. How can that be?

Morphogens play a key role in development, creating concentration gradients that inform cells of where they are and how to behave. Examine the simple patterns represented by the flags in Figure Q211. Which do you suppose could be created by a gradient of a single morphogen? Which would require gradients of two morphogens? Assuming that such patterns were present in a sheet of cells, explain how they could be created by morphogens.

Two adjacent cells in the nematode worm normally differentiate into an anchor cell (AC) and a ventral uterine precursor (VU) cell, but which of the two becomes the AC and which becomes the VU cell is completely random: the cells have an equal chance of adopting either fate, but they always adopt different fates. Mutations of Lin12 alter these fates. In hyperactive Lin12 mutants, both cells become VU cells, while in inactive Lin12 mutants, both cells become ACs. Thus, Lin12 is central to the decision-making process. In genetic mosaics in which one precursor cell has the hyperactive Lin12 and the other precursor has the inactive Lin12, the cell with the hyperactive Lin12 always becomes the VU cell and the cell with inactive Lin12 always becomes the AC. Assuming that one cell sends a signal and the other cell receives it, explain how these results suggest that Lin12 encodes a protein required to receive the signal. Offer a suggestion for how the fates of these two precursor cells are normally decided in wildtype worms.

It was clear from the early days of studying development that certain morphogenetic substances were present in the egg and segregated asymmetrically into cells of the developing embryo. One such investigation in ascidian (sea squirt) embryos examined endodermal alkaline phosphatase, which could be visualized by a histochemical stain. Treatment of embryos with cytochalasin B stopped cell division, but did not block expression of alkaline phosphatase at the appropriate time. Treatment with actinomycin D, which blocks transcription, did not interfere with expression of alkaline phosphatase. Treatment with puromycin, which blocks translation, eliminated expression of alkaline phosphatase. What is the likely nature of the morphogenetic substance that gives rise to alkaline phosphatase?

The mouse HoxA3 and HoxD3 genes are paralogs that occupy equivalent positions in their respective Hox gene clusters and share roughly 50% identity in their protein-coding sequences. Mice with defects in HoxA3 have deficiencies in pharyngeal tissues, whereas mice with defects in HoxD3 have deficiencies in the axial skeleton, suggesting quite different functions for the paralogs. Thus, it came as a surprise when it was found that replacing a defective HoxD3 gene with the normal HoxA3 gene corrected the deficiency, as did the reciprocal experiment of replacing a mutant HoxA3 gene with a normal HoxD3 gene. Neither transplaced gene, however, could supply its normal function; that is, a normal HoxA3 gene at the HoxD3 locus could not correct the deficiency caused by a mutant HoxA3 gene at the HoxA3 locus. The same was true for the HoxD3 gene. If the HoxA3 and HoxD3 genes are equivalent, how do you suppose they can play such distinct roles in development? Why do you suppose they cannot perform their normal function in a new location?

The segmentation of somites in vertebrate embryos is thought to depend on oscillations in the expression of the Hes7 gene. Mathematical modeling explains these oscillations in terms of the delays in production of the unstable Hes7 protein, which acts as a transcription regulator to shut off its own expression. Once Hes7 decays, with a halflife of about 20 minutes, its transcription resumes. To test this model, you decide to reduce the total delay by removing one, two, or all three of the introns from the Hes7 gene in mice. Why do you expect that intron removal would reduce the delay? What would you predict would happen to the oscillation time, and somite formation, if the model were correct?

The oscillatory clock that drives somite formation in vertebrates involves three essential components Her7 (an unstable repressor of its own synthesis), Delta (a transmembrane signaling molecule), and Notch (a transmembrane receptor for Delta). Notch is bound by Delta on neighboring cells, activating the Notch signaling pathway, which then activates Her7 transcription. Normally, this system works flawlessly to create sharply defined somites (Figure Q212A). In the absence of Delta, however, only the first five somites form normally, and the rest are poorly defined (Figure Q212B). If a pulse of Delta is supplied later, somite formation returns to normal in the regions where Delta was present (Figure Q212C). A diagram of the connections between the components of the clock and how they interact in adjacent cells is shown in Figure Q212D. In the absence of Delta, why do the cells become unsynchronized? What is it about the presence of Delta that keeps adjacent cells oscillating in synchrony?

The extracellular protein factor Decapentaplegic (Dpp) is critical for proper wing development in Drosophila (Figure Q213A). It is normally expressed in a narrow stripe in the middle of the wing, along the anteriorposterior boundary. Flies that are defective for Dpp form stunted wings (Figure Q213B). If an additional copy of the gene is placed under control of a promoter that is active in the anterior part of the wing, or in the posterior

The highly branched structures of neurons would seem to make it almost inevitable that they should make unproductive synapses with themselves, yet they manage to avoid this outcome very effectively. How is this accomplished in vertebrates?