Interesting phenotypes found in male-female mosaic mutations of the silkworm are thought to result from the abnormal activation of a polar body due to the defect on the inactivation system. In addition to these mosaic mutations, a parthenogenetic strain (m90) of silkworm has been identified. The precise mechanism of parthenogenetic development in this strain is unknown, but it is possible that a defect of the polar body inactivation system plays a crucial role here, too. To understand the molecular mechanisms of polar body inactivation, we investigated the process of artificial and spontaneous parthenogenetic development using the mosaic mutations and the m90 strain. Both the pigmentation and the increase in DNA content were used to monitor development. In order to determine whether parthenogenesis in these strains is caused by incomplete meiotic division or fertilization of a polar body with the egg nucleus, the chromosome compositions were analyzed using an insertion sequence in the testis-specific tektin gene as a molecular marker. It was confirmed that parthenogenesis in the mosaic mutations was partly caused by the fertilization of a polar body nucleus with the egg nucleus. In contrast, parthenogenetic development in the m90 strain is apparently caused by incomplete meiotic division.
All Science Journal Classification (ASJC) codes
- Animal Science and Zoology
- Developmental Biology