Mitosis in Drosophila development

Abstract

SummaryMany aspects of the mitotic cycle can take place independently in syncytial Drosophila embryos. Embryos from females homozygous for the mutation gnu undergo rounds of DNA synthesis without nuclear division to produce giant nuclei, and at the same time show many cycles of centrosome replication (Freeman et al. 1986). S phase can be inhibited in wild-type Drosophila embryos by injecting aphidicolin, in which case not only do centrosomes replicate, but chromosomes continue to condense and decondense, the nuclear envelope undergoes cycles of breakdown and reformation, and cycles of budding activity continue at the cortex of the embryo (Raff and Glover, 1988). If aphidicolin is injected when nuclei are in the interior of the embryo, centrosomes dissociate from the nuclei and can migrate to the cortex. Pole cells without nuclei then form around those centrosomes that reach the posterior pole (Raff and Glover, 1989); the centrosomes presumably must interact with polar granules, the maternally-provided determinants for pole cell formation. T he pole cells form the germ-line of the developing organism, and as such may have specific requirements for mitotic cell division. This is suggested by our finding that a specific class of cyclin mRNAs, the products of the cyclin B gene, accumulate in pole cells during embryogenesis (Whitfield et al. 1989). Other genes that are essential for mitosis in early embryogenesis and in later development are discussed.

Modelling Malignant Progression with a Finite State Machine Supports a Two Checkpoint Theory of Cancer

“…First, a high proportion of aneuploid cells will die because they lack genes that are essential for survival. Following an unequal distribution of chromosomes at cell division, the spontaneous cell loss factor is usually at least 50%, and may be greater than 90% [16]. The aneuploid cells that contain all the genes essential for survival can then go into successive cell divisions without excessive cell loss.…”

Developmental defects observed in hypomorphic anaphase-promoting complex mutants are linked to cell cycle abnormalities

“…The APC/C then promotes mitotic exit by ubiquitinating the M-phase cyclins (reviewed by Morgan, 1999). More recently, the APC/C has been shown to function in separating paired homologs during meiosis I (Cooper et al, 2000;Davis et al, 2002;Furuta et al, 2000;Golden et al, 2000) and sister chromatids during meiosis II (Peter et al, 2001;Taieb et al, 2001). To date, SnoN, a negative regulator of TGFβ signaling (Stroschein et al, 2001;Wan et al, 2001) is the only documented non-cell cycle target of the APC/C.…”

“…In fact, the late-developing everted vulva phenotype in emb-30/apc-4 mutants, and presumably other APC/C mutants, has been shown to be associated with extended M-phase delays and variable lineage truncations within the vulva cell lineage (Furuta et al, 2000). In a different multicellular context, the C. elegans germline is a highly proliferative tissue, which like the germline and imaginal discs in Drosophila, is particularly sensitive to cell cycle defects (Albertson et al, 1978;Glover, 1989). Given that the 1000+ cells that compose the mature, syncytial germline arise from just two cells within hatching L1 larva (Hirsh et al, 1976), it is not surprising that many APC/C mutants develop severely reduced germlines due to mitotic defects (Furuta et al, 2000;Golden et al, 2000).…”

“…In a different multicellular context, the C. elegans germline is a highly proliferative tissue, which like the germline and imaginal discs in Drosophila, is particularly sensitive to cell cycle defects (Albertson et al, 1978;Glover, 1989). Given that the 1000+ cells that compose the mature, syncytial germline arise from just two cells within hatching L1 larva (Hirsh et al, 1976), it is not surprising that many APC/C mutants develop severely reduced germlines due to mitotic defects (Furuta et al, 2000;Golden et al, 2000). Lastly, the powerful combination of excellent cytology, well-established genetics and RNA interference (RNAi) methodology can be used to analyze how the APC/C functions at the cellular level to support cell cycle progression and development of the C. elegans zygote.…”

The Role of Model Organisms in the History of Mitosis Research

“…Drosophila is an attractive organism in which to study both the rapid rounds of mitosis typical of embryonic development and the longer cell cycles of diploid tissues later in development (Glover 1989). Powerful molecular biological studies of fruit fly mitosis became possible after the discovery of Drosophila mutants and use of reagents, pioneered by Nuesslein-Volhard (St Johnston and Nuesslein-Volhard 1992).…”