Fig 2: (A to E) Growth phenotypes of S. marcescens PIC3611 on 0.2% (wt/vol) glucose (A), 0.25% (wt/vol) N-acetylglucosamine (B), 1% (wt/vol) a-chitin (C), 5% (wt/vol) crab shell (Callinectes sapidus) (D), and 5% (wt/vol) fungal biomass (Aspergillus nidulans) (E) as the sole carbon sources. (F) Chitinase secretion of S. marcescens PIC3611 on 0.5% (wt/vol) colloidal chitin as the sole carbon source, as shown by Congo red staining. All media and plates were made with MOPS minimal medium and supplemented with the designated carbon source. All growth experiments were completed in biological triplicate, with error bars representing standard deviations, although some are too small to be observed. Growth analyses on glucose and N-acetylglucosamine were completed in an EPOCH2 microplate reader (BioTek), while growth on a-chitin, fungal biomass, and crab shell were measured using test tubes and a spectrophotometer (Milton Roy Spec20D+).

Fig 3: CCND2 plays a role in prostate cancer cell proliferation. (a) Ectopic expression of CCND2 in LNCaP inhibits its cellular proliferation. Left: Measurement of CCND2 overexpression by Western blot. Note that the three lanes represent LNCaP without transfection, LNCaP transfected with empty vector and LNCaP transfected with CCND2 expression plasmids, respectively. Right: The results of MTT in LNCaP cells upon CCND2 overexpression. Comparing to controls (no transfection or transfection with empty vector), the proliferations of LNCaP cells were significantly inhibited. The absorbance at 570 nm was measured with EPOCH2 Microplate Readers (BioTek), mean ± s.d. of four independent experiments. (b) Knockdown of CCND2 in DU145 promotes its cellular proliferation. Left panel: The knockdown efficiency of siRNAs against CCND2 were measured by quantitative real-time PCR. Right panel: Knockdown of CCND2 increases cell proliferation of prostate cancer DU145 cell line measured by XTT colorimetric assay (absorbance at 450 nm (OD450); mean ± s.d. of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. In (a and b), the P values were assessed by the two-tailed Student’s t test. (c,d) Expression correlation of CCND2 with MKI67 in human prostate tumor samples. Scatter plot showing the inverse correlation between CCND2 and MKI67 expression in two independent cohorts of prostate tumors (n = 131 and n = 264, respectively)30, 31.

Fig 4: Osmostress protection assay with 5-hydroxyectoine and 5-hydroxyhomoectoine. Growth of E. coli MG1655 (proU+ proP+) in MMA without NaCl and in MMA containing 0.8 M NaCl without and with the addition of 1 mM of the indicated compatible solutes was monitored for 60 h. The OD578 of the cultures was measured hourly in a plate reader (Epoch2, BioTek). The osmostress protection growth assay was conducted with two independently grown cultures. A representative set of growth curves is shown.

Fig 5: Phenotype changes in evolved aneuploid yeast lines.a Doubling time of ancestor and evolved lines. Cells were grown at 30 °C, and OD600 measurements were taken at 15 min intervals using a Biotek-Epoch2 instrument until the cells reached early stationary phase. Doubling time was calculated with a custom R script by analyzing fitting spline function from growth curve slopes. Bar graphs represent mean of three measurement and error bars are SEM. Red bars represent the doubling time of ancestor strains for both WT and disomes. Black bars show the doubling time of evolved lines for corresponding strains. Mean values are shown; error bars represent SD. Source data for doubling times is presented as source data file. b Color changes from red to white in evolved lines.