Table 1.

Effects on the cell surface by individual component disruption

Altered componenta
	PG	CPS	WTA	LTA
PG	Abnormal morphology [16] Assymetric septum [16] Increased autolysis [15] Increased chain length [15]	Increased sensitivity to antimicrobials [36,37] Altered chain length [39,40]	Increased autolysis [32] Decreased lysozyme resistance [25] Decreased PG crosslinking [23,25] Perturbation of PG [23] Aberrant morphology [23]	Decreased autolysis [26] Abnormal morphology [28] Aberrant cell division [26] Increased chain length [28]
CPS	Covalent attachment of CPS to PG [7,34,35]	Not considered [7]	Increased levels of CPS [33]	Unknown
WTA	Covalent attachment of WTA to PG [5]	Increased levels of WTA [33]	Not considered [30,3]	Can compensate for essential function of LTA [5,26]
LTA	β-lactam treatment causes release of LTA [42]	Unknown	Can compensate for essential function of WTA [5,26]	Not considered [3,30]

^aA collection of phenotypes exhibited when components at the top are disrupted in some way in relation to the other components of the cell surface. Categories “Not considered” were judged to be outside the scope of this summary and have been described at length in the associated citation. Categories that are “Unknown” did not have significant findings to present in this context.