TY - JOUR
T1 - Mutations at the fat locus interfere with cell proliferation control and epithelial morphogenesis in Drosophila
AU - Bryant, Peter J.
AU - Huettner, Beth
AU - Held, Lewis I.
AU - Ryerse, Jan
AU - Szidonya, János
N1 - Funding Information:
This work was supported by Grant HD06082 from NIH to Peter Bryant, Grant DCB-8517532 from NSF to Lewis Held, and gifts from the Monsanto Company to Peter Bryant and Jan Ryerse. We thank Becky Hsei, Laura Wilson, and Marjorie Boyette for technical assistance. James Ng did the cell counts.
PY - 1988/10
Y1 - 1988/10
N2 - Lethal mutations at the fat locus in Drosophila cause imaginal discs to continue to grow by cell proliferation far beyond their normal final size. During a greatly extended larval period, the overgrowing imaginal discs develop additional folds and lobes, but retain a single-layered epithelial structure. In the wing disc, the additional lobes originate in the proximal fold area, and in the extra tissue the cells are less columnar than normal. Mutant disc cells lack zonulae adherents as well as associated microtubules and microfilaments, and they show an abnormal distribution and reduced density of gap junctions. The effect on growth is disc-autonomous as shown by transplantation experiments. The overgrown imaginal discs retain the ability to differentiate adult cuticular structures, as shown by metamorphosis of discs after transplantation into wild-type larval hosts and by the ability of some mutant animals to develop to the pharate adult stage. The structures differentiated by mutant discs show many abnormalities including ingrowths, outgrowths, separated cuticular vesicles, and areas of reversed bristle polarity; some of these abnormalities suggest that the mutations interfere with cell adhesion as well as the control of cell proliferation. The fat locus is located in cytogenetic interval 24D5.6-7, and 18 alleles are known including spontaneous, chemically induced, X-ray-induced, and dysgenic mutations.
AB - Lethal mutations at the fat locus in Drosophila cause imaginal discs to continue to grow by cell proliferation far beyond their normal final size. During a greatly extended larval period, the overgrowing imaginal discs develop additional folds and lobes, but retain a single-layered epithelial structure. In the wing disc, the additional lobes originate in the proximal fold area, and in the extra tissue the cells are less columnar than normal. Mutant disc cells lack zonulae adherents as well as associated microtubules and microfilaments, and they show an abnormal distribution and reduced density of gap junctions. The effect on growth is disc-autonomous as shown by transplantation experiments. The overgrown imaginal discs retain the ability to differentiate adult cuticular structures, as shown by metamorphosis of discs after transplantation into wild-type larval hosts and by the ability of some mutant animals to develop to the pharate adult stage. The structures differentiated by mutant discs show many abnormalities including ingrowths, outgrowths, separated cuticular vesicles, and areas of reversed bristle polarity; some of these abnormalities suggest that the mutations interfere with cell adhesion as well as the control of cell proliferation. The fat locus is located in cytogenetic interval 24D5.6-7, and 18 alleles are known including spontaneous, chemically induced, X-ray-induced, and dysgenic mutations.
UR - http://www.scopus.com/inward/record.url?scp=0024094911&partnerID=8YFLogxK
U2 - 10.1016/0012-1606(88)90399-5
DO - 10.1016/0012-1606(88)90399-5
M3 - Article
C2 - 3417051
AN - SCOPUS:0024094911
SN - 0012-1606
VL - 129
SP - 541
EP - 554
JO - Developmental Biology
JF - Developmental Biology
IS - 2
ER -