Thus, miRNAs can sharpen developmental transitions by blocking and removing mRNAs that define an earlier developmental stage. But how is the timing of miRNA expression itself controlled? In the case of the miRNAs that disable maternal mRNAs in frogs and fish, expression is activated at the end of the series of rapid, synchronous divisions that cleave the fertilized egg into many smaller cells. As the division rate of these blastomeres slows, widespread transcription of the embryo’s genome begins (Figure 21–43). This event, where the embryo’s own genome largely takes over control of development from maternal macromolecules, is called the maternal-zygotic transition (MZT), and it occurs with roughly similar timing in most animal species, with the exception of mammals.
One trigger for the MZT appears to be the nuclear-to-cytoplasmic ratio. During cleavage, the total amount of cytoplasm in the embryo remains constant, but the number of cell nuclei increases exponentially. As a critical threshold is reached in the ratio of cytoplasm to DNA, the cell cycles lengthen and transcription is initiated. Thus, haploid embryos undergo the MZT one cell cycle later than diploid embryos, which contain twice as much DNA per cell. According to one
Figure 21–43 The maternal-zygotic transition in a zebrafish embryo.
Maternal mrNas are deposited by the mother into the egg and drive early development. these mrNas are degraded during different stages of embryogenesis, including blastula and gastrula stages, but a relatively abrupt change occurs at the maternal-zygotic transition (MZt). Before this, the embryonic (zygotic) genome is transcriptionally inactive; afterward, zygotic model, the nuclear-to-cytoplasmic ratio might be measured through the titration of a transcription repressor against the increasing amount of nuclear DNA. The total amount of repressor would stay constant during cleavage divisions, but the amount of repressor per genome would decrease, falling by a half with each round of DNA synthesis, until loss of repression allowed the zygotic genome to become transcriptionally active. The newly synthesized transcripts include the miRNAs that recognize many of the transcripts deposited in the egg by the mother, directing their translational repression and rapid degradation.
hormonal Signals coordinate the timing of Developmental transitions
We have so far emphasized timing mechanisms that operate locally and separately in the different parts of the embryo, or in specific subsystems of the molecular control machinery. Evolution has tuned each of these largely independent processes to run at an appropriate rate, matched to the needs of the organism as a whole. For some purposes, however, this is not enough: a global coordinating signal is required. This is especially true where changes have to occur throughout the body in response to a cue that depends on the environment. For example, when an insect or amphibian undergoes metamorphosis—the transition from larva to adult—almost every part of the body is transformed. The timing of metamorphosis depends on external factors such as the supply of food, which determines when the animal reaches an appropriate size. All the bodily changes have to be triggered together at the right time, even though they are occurring in widely separated sites. The coordination in such cases is provided by hormones—signal molecules that spread throughout the body.
The metamorphosis of amphibians provides a spectacular example. During this developmental transition, amphibians switch from an aquatic to a terrestrial life. Larva-specific organs such as gills and tail disappear, and adult-specific organs such as legs form. This dramatic transformation is triggered by thyroid hormone, produced in the thyroid gland. If the gland is removed or if thyroid hormone action is blocked, metamorphosis does not occur, although growth continues, producing a giant tadpole. Conversely, a dose of thyroid hormone given to a tadpole by an experimenter can trigger metamorphosis prematurely.