QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nakato, H. Articles by Selleck, S. B. Search for Related Content PubMed PubMed Citation Articles by Nakato, H. Articles by Selleck, S. B.

dally, a Drosophila member of the glypican family of integral membrane proteoglycans, affects cell cycle progression and morphogenesis via a Cyclin A-mediated process

Department of Molecular and Cellular Biology, and The Arizona Cancer Center, Salmon Building, Rm 0975, 1515 N. Campbell Avenue, University of Arizona, Tucson, AZ 85724, USA

View larger version (32K): [in a new window]   Fig. 1. Eye phenotypes of dally mutants are rescued by reducing cycA function. Each dallyP2 adult was scored for eye defects and classified into ‘mild’, ‘moderate’, or ‘severe’ based on the degree of reduction in the number of ommatidia. Animals heterozygous for cycA3 showed approximately a threefold decrease in the number of animals with the severe class of defect compared with dally mutants wild-type for cycA (n=215 for dally/dally; n=187 for dally cycA/dally +).

View larger version (53K): [in a new window]   Fig. 2. Cell division defects in LPCs of dally mutants are rescued by reducing cyclin A expression. (A) Lateral views of brain lobes from dallyP2/TM6B (top left), dallyP2/dallyP2 (top right) and dallyP2 cycA3/dallyP2 (bottom left). cycB/+; dallyP2/dallyP2 (bottom right) third instar larvae are shown stained with anti-cyclin B antibody. The two LPC divisions are seen as two stripes of immuno-positive cells (marked 1 and 2) at the anterior edge of the lamina (LA). Note that the second domain of Cyclin B-positive cells, absent in dallyP2/dallyP2, is observed in the dallyP2 cycA3/dallyP2 preparation. We confirmed that cycB/+ animals show reduced levels but normal patterns of Cyclin B protein expression (data not shown). (B) Quantitative analysis of LPC division rescue by cycA. Third instar larval brains were stained with anti-Cyclin B antibody and scored for the percentage of LPCs showing the second stripe of Cyclin B expression. Each closed circle represents a single larval brain serially sectioned by confocal microscopy, and scored without knowledge of the genotype. cycA5 showed similar effects to cycA3 on expression of LPC division phenotype in dally mutants (data not shown).

View larger version (89K): [in a new window]   Fig. 3. Reducing string expression does not rescue dally LPC division phenotypes. Anti-cyclin A staining patterns of LPCs and lamina (LA) in dallyP2/TM6B (A), dallyP2/dallyP2 (B) and dallyP2 stg7B/dallyP2 (C) larval brains. Deleting one functional copy of stg does not rescue the second LPC division, and appears to expand the first G2/M domain of LPC division in dally mutants.

View larger version (139K): [in a new window]   Fig. 4. Abnormal expression of Cyclin A in larval brains of dally mutants. Lateral views of LPCs and lamina (LA) of dally heterozygous (dallyP2/TM6B, A-C) or homozygous (dallyP2/dallyP2, D-F) larval brains stained with anti-cyclin A antibody (red, A,D) and propidium iodide (gray tones, B,E). C and F show merged images of A and B, and D and E, respectively. The numbers 1 and 2 in A mark the two consecutive LPC divisions that occur in front of and immediately posterior to the lamina furrow in a wild-type brain, respectively. The arrow marks a dividing cell in the first LPC division where loss of Cyclin A immunoreactivity is associated with entry into M phase, as shown by the condensed state of the chromosomes (A,B). The second LPC division cycle is completely absent in the dally mutant brain lobe, as shown by the lack of Cyclin A expression posterior to the lamina furrow. Arrows in D-F indicate cells in dally mutant brains that show condensed chromosomes, yet retain high levels of Cyclin A immunoreactivity.

View larger version (108K): [in a new window]   Fig. 5. Pattern of Cyclin A expression in wild-type and dally LPCs. A series of wild-type and dally mutant LPCS in M phase are shown, stained with anti-Cyclin A antibody (red) and propidium iodide (gray scale) to visualize the condensation state of chromosomes. Left panels show Cyclin A staining, middle panels show propidium iodide staining of chromosomes, and the right panels are merges of Cyclin A and propodium iodide images. The top six panels show wild-type LPCs. The arrowheads mark cells where Cyclin A has been degraded and propidium iodide staining shows the cells are in prophase, where chromosome condensation has begun, but not yet achieved the alignment indicative of metaphase. The arrow marks a cell in prophase that retains some residual level of Cyclin A immunoreactivity. dally mutant LPCs show a very different pattern of Cyclin A immunoreactivity in M phase. Shown are several LPCs (arrows) with significant levels of Cyclin A and highly condensed chromosomes characteristic of metaphase. In wild-type Cyclin A immunoreactivity is never seen in LPCs with this degree of chromosome condensation.