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Fig. 7. Cell autonomous defects of the dimA– mutant. (A)
Development on DIF-agar. 100 nM DIF-1 slightly slows the development of the
wild type as some tip mounds are still visible up to 15 hours (a,b), although
all structures ultimately fruit normally (c). dimA–
development is unaffected by the addition of exogenous DIF-1, as slugs remain
long and thin (d,e) with a tendency to break (arrowhead), and fruiting bodies
still lie on the surface of the agar (f). By contrast, 100 nM DIF-1 is
sufficient to rescue the phenotype of the dmtA–
mutant, as both slugs (g,h) and fruiting bodies (i) appear normal. (B)
dimA– cell-autonomous defects in chimeras with
wild-type cells. Wild-type or dimA– mutant cells
were transformed with the constitutively expressed
actin15/lacZ marker and mixed with unlabeled cells. (a,b)
Control samples illustrate that expression of the marker itself does not
affect cell fate or position (c) Labeled AX4 cells localize to the pstO and
anterior prespore zones in chimeras with unlabeled
dimA– mutant cells. (d) Labeled
dimA– mutant cells are strongly enriched in the
posterior prespore zone in chimeras with unlabeled wild-type cells. (C)
Expression of the cotB/lacZ prespore marker in chimeric slugs. (a)
cotB/lacZ-expressing AX4 cells are scattered throughout the
prespore zone of chimeras with unmarked dimA– cells.
(b) dimA– cells that express the
cotB/lacZ prespore marker are predominantly found at the
rear of the prespore zone in chimeras with unmarked wild-type cells.
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