TY - JOUR
T1 - Cell adhesion and fluid flow jointly initiate genotype spatial distribution in biofilms
AU - Martínez-García, Ricardo
AU - Nadell, Carey D.
AU - Hartmann, Raimo
AU - Drescher, Knut
AU - Bonachela, Juan A.
PY - 2018/4/16
Y1 - 2018/4/16
N2 - Biofilms are microbial collectives that occupy a diverse array of surfaces. It is well known that the function and evolution of biofilms are strongly influenced by the spatial arrangement of different strains and species within them, but how spatiotemporal distributions of different genotypes in biofilm populations originate is still underexplored. Here, we study the origins of biofilm genetic structure by combining model development, numerical simulations, and microfluidic experiments using the human pathogen Vibrio cholerae. Using spatial correlation functions to quantify the differences between emergent cell lineage segregation patterns, we find that strong adhesion often, but not always, maximizes the size of clonal cell clusters on flat surfaces. Counterintuitively, our model predicts that, under some conditions, investing in adhesion can reduce rather than increase clonal group size. Our results emphasize that a complex interaction between fluid flow and cell adhesiveness can underlie emergent patterns of biofilm genetic structure. This structure, in turn, has an outsize influence on how biofilm-dwelling populations function and evolve.
AB - Biofilms are microbial collectives that occupy a diverse array of surfaces. It is well known that the function and evolution of biofilms are strongly influenced by the spatial arrangement of different strains and species within them, but how spatiotemporal distributions of different genotypes in biofilm populations originate is still underexplored. Here, we study the origins of biofilm genetic structure by combining model development, numerical simulations, and microfluidic experiments using the human pathogen Vibrio cholerae. Using spatial correlation functions to quantify the differences between emergent cell lineage segregation patterns, we find that strong adhesion often, but not always, maximizes the size of clonal cell clusters on flat surfaces. Counterintuitively, our model predicts that, under some conditions, investing in adhesion can reduce rather than increase clonal group size. Our results emphasize that a complex interaction between fluid flow and cell adhesiveness can underlie emergent patterns of biofilm genetic structure. This structure, in turn, has an outsize influence on how biofilm-dwelling populations function and evolve.
KW - planktonic cells
KW - bacteria
KW - biofilms
KW - cell adhesion
UR - http://www.scopus.com/inward/record.url?scp=85046366221&partnerID=8YFLogxK
U2 - 10.1371/journal.pcbi.1006094
DO - 10.1371/journal.pcbi.1006094
M3 - Article
AN - SCOPUS:85046366221
SN - 1553-734X
VL - 14
JO - PLoS Computational Biology
JF - PLoS Computational Biology
IS - 4
M1 - e1006094
ER -