The two regulatory pathways appear to come together at the IME1 gene. It is clearly regulated by mating type and induced by starvation as well. Overexpression of IME1 completely overcomes MAT defects but may not circumvent all nutritional control. Kassir et al. (1988) found that overexpression of IME1 allowed sporulation in the presence of glucose and nitrogen. They also have found a meiotic level of message in temperature-sensitive cdc25 diploids shifted to high temperature in rich medium (Simchen and Kassir, 1989). Smith and Mitchell (1989) found that overexpression of IME1 induced an early meiotic event (recombination) in rich medium, but later meiotic events did not occur (i.e., they detected no spore formation). Mitchell (personal communication) has suggested that the difference may be due to differences in the amount of nitrogen present in the two experiments. Thus, while it is clear that IME1 is a necessary positive regulator of meiosis, responding both to mating type and nutritional conditions, it is not clear if it is sufficient. It is possible that other genes are involved in the response to starvation. One interpretation is that a separate nutritional control is exerted for events starting with meiosis I. Much of the regulatory pathway that allows yeast cells to enter meiosis has been determined. As in the case in many sensory transduction pathways, the initial signal for starvation is not yet known, nor is the nature of the proposed downstream phosphorylated effector. Given the power of yeast molecular genetics, answers to both these questions seem attainable. Another area that remains unclear is the difference between responses to nitrogen starvation versus carbon source. Many of the experiments discussed above do not address this question. The strategies used by yeast may be utilized in the developmental decisions used by other, more complex eukaryotes. Certainly several of the gene products involved in nutritional control in yeast have homologies in mammalian systems. For example, the human H-ras gene can substitute for yeast RAS; the relationship is sufficiently close that dominant Ha-ras mutations that inhibit CDC25 have been found (Powers et al., 1989). Furthermore, these dominant Ha-ras mutations have the appropriate phenotype in mammalian cells, suggesting the presence of a CDC25-like protein. Although the major components of mating type control appear to have been defined, the mechanism of the RME1-IME transcriptional control remains to be determined.(ABSTRACT TRUNCATED AT 400 WORDS)