Chapter 18: Problem 5
Distinguish between the syncytial blastoderm stage and the cellular blastoderm stage in Drosophila embryogenesis.
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Chapter 18: Problem 5
Distinguish between the syncytial blastoderm stage and the cellular blastoderm stage in Drosophila embryogenesis.
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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?
The identification and characterization of genes that control sex determination has been a focus of investigators working with \(C .\) elegans. As with Drosophila, sex in this organism is determined by the ratio of \(X\) chromosomes to sets of autosomes. A diploid wild-type male has one \(X\) chromosome and a diploid wild-type hermaphrodite has two X chromosomes. Many different mutations have been identified that affect sex determination. Loss- of-function mutations in a gene called her-1 cause an XO nematode to develop into a hermaphrodite and have no effect on \(\mathrm{XX}\) development. (That is, \(\mathrm{XX}\) nematodes are normal hermaphrodites.) In contrast, loss- offunction mutations in a gene called tra-I cause an XX nematode to develop into a male. Deduce the roles of these genes in wild-type sex determination from this information.
Much of what we know about gene interactions in development has been learned using nematodes, yeast, flies, and bacteria. This is due, in part, to the relative ease of genetic manipulation of these well-characterized genomes. However, of great interest are gene interactions involving complex diseases in humans. Wang and White (2011. Nature Methods 8(4) \(341-346\) ) describe work using RNAi to examine the interactive proteome in mammalian cells. They mention that knockdown inefficiencies and off-target effects of introduced RNAi species are areas that need particular improvement if the methodology is to be fruitful. (a) How might one use RNAi to study developmental pathways? (b) Comment on how "knockdown inefficiencies" and "off-tar-get effects" would influence the interpretation of results.
In Arabidopsis, flower development is controlled by sets of homeotic genes. How many classes of these genes are there, and what structures are formed by their individual and combined expression?
The apterous gene in Drosophila encodes a protein required for wing patterning and growth. It is also known to function in nerve development, fertility, and viability. When human and mouse genes whose protein products closely resemble apterous were used to generate transgenic Drosophila (RinconLimas et al. \(1999 .\) Proc. Nat. Acad. Sci. \([\mathrm{USA}] 96: 2165-2170\) ) the apterous mutant phenotype was rescued. In addition, the whole-body expression patterns in the transgenic Drosophila were similar to normal apterous. (a) What is meant by the term rescued in this context? (b) What do these results indicate about the molecular nature of development?
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