Lumbar lateral motor column development in triploid Xenopus laevis

The effects of increasing ploidy on the development of the lumbar lateral motor column (L‐LMC) in Xenopus laevis were investigated in order to determine how early events contribute to producing the significant difference in the average number of motoneurons present in diploid and triploid animals after cell death (Sperry: J. Comp. Neurol. 277: 499–508, '88). From naturally occurring diploid and experimentally produced triploid siblings at two stages prior to significant amounts of neuronal cell death, at one stage during the peak period of cell death, and at one stage after cell death, the L‐LMC motoneurons were counted and nuclear cross‐sectional areas were measured. At stages before and after cell death, the average nuclear crosssectional areas of motoneurons and of other cells that were also measured were greater in the triploids, while the average number of motoneurons and motoneuron density (the mean number of cells per section) were less. Average body size and average motor column length in diploid and triploid animals were equal at each of the stages. The general characteristics of L‐LMC development that have been widely noted in diploids, an increase in cell size accompanied by a decrease in cell number, were also observed in the triploid animals. However, not only were these general features present in the triploids, but the increase in average motoneuron size and the decrease in average motoneuron number in diploids and triploids were roughly equal when scaled to the general differences in nuclear size or to the difference in the average number of motoneurons present prior to cell death. There was no evidence that the triploid condition affected the magnitude of the cell death process. Overall, the findings suggest that the processes underlying L‐LMC development in experimentally produced triploids may not be different from those in naturally occurring diploids. The smaller average numbers of motoneurons after cell death in the triploids may be related to some feature of the triploid condition that affects the number of motoneurons present before cell death rather than to a feature of the triploid animals, such as peripheral size, that is thought to affect the motoneuron cell death process itself. The relationship of these findings to the general issue of how the size of the L‐LMC motoneuron population in triploids, as well as in diploids, might be regulated is discussed.