“…In spite of the versatile pathogenic potential of F. nucleatum , little is known about the mechanisms of fusobacterial virulence and associated factors, and virtually nothing is known about many other basic cellular processes in F. nucleatum , including protein transport, cell surface biogenesis, and cell division or cytokinesis. To date, less than a dozen of fusobacterial factors have been reported; these factors include FomA, FadA, Fap2, RadD, Aid1, FAD-I, and CmpA ( 6 , 8 – 16 ), although more than 2,000 open reading frames (ORFs) are annotated in the genomes of many F. nucleatum strains ( 17 – 20 ) (see also https://www.patricbrc.org/ ). The majority of the aforementioned factors are adhesins, with Fap2, RadD, Aid1, and CmpA involved in polymicrobial interactions or coaggregation ( 10 – 12 , 16 ); among these, only RadD and CmpA have been implicated in biofilm formation ( 10 , 16 ).…”