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. 1999 Oct;10(10):3301–3316. doi: 10.1091/mbc.10.10.3301

Figure 5.

Figure 5

Mutations in mitotic control genes modulate filamentous differentiation. The clb2/clb2 mutant exhibits exaggerated filamentous development and a growth pattern similar to that of the STE11-4 mutant. (A) Both the strain carrying the ts mitotic arrest allele cdc28-1N and the strain deficient in CLB2 exhibit filamentous growth on YPD media and are further induced by nitrogen starvation. Photographs show representative colonies of each strain after 24 h at 22°C. (B) Agar invasion assay. Cells lacking CLB2 have enhanced YPD agar invasion comparable to that displayed by the STE11-4 mutant. (C) Cell morphology in liquid YPD media. The clb2/clb2 strain grows as highly elongated cells that remain attached in clusters, reminiscent of the STE11-4 mutant. Bars, 50 μm. (D) Cell cycle kinetics. Like STE11-4 cells, CLB2-deficient cells demonstrate a predominance of cells with G2/M DNA content. (E) Deficiency in mitotic Cdc28 activity conferred by deficiency in the Clb2 mitotic cyclin dramatically enhances filamentous growth on both synthetic nitrogen (SC) and nitrogen starvation (SLAD) media. Activation of the RAS/STE pathway via plasmids containing STE11-4 or RAS2-Val19 augments the striking cell elongation phenotype of these strains. Bars, 50 μm.