Table 2.

Biogenesis of the major cell envelope components of M. tuberculosis H37Rv.

Biosynthetic pathway	# Genes	Evidence			# Refs
		Phenotypic	Enzymatic	Homology
Non-mevalonate isopentenyl diphosphate synthesis	5	0	5	0	12
Prenyl diphosphate synthases	4	0	4	0	7
Peptidoglycan synthesis and turnover / cell division	69	28	24	34	89
Arabinogalactan synthesis	28	10	22	0	33
Fatty acids, mycolic acids, TMM and TDM (synthesis, transport, regulation, and processing)	66	31	30	27	67
Phospholipid biosynthesis	6	1	2	4	2
Triglyceride biosynthesis	16	2	16	0	3
PIM, LM and LAM biosynthesis	13	13	10	0	24
Methylglucose lipopolysaccharides*, glycogen* and capsular α-glucans	13	9	7	3	13
Polymethylbranched fatty acid-containing acyltrehaloses	12	11	5	1	10
Phthiocerol dimycocerosates, phenolic glycolipids and p-hydroxybenzoic acid derivatives	27	27	9	0	31
Mannosyl-β-1-phosphomycoketides	1	1	1	0	2

The number of genes that were annotated per major biosynthetic pathways during the TB CAP exercise, and the evidence and number of PMID references on which the annotation was based are shown. The experimental evidence for the annotation of a gene may either be ‘enzymatic’ (i.e., an enzymatic activity was associated to the gene's product in vitro) or ‘phenotypic’ (i.e., the annotation results from the biochemical analysis of mycobacterial recombinant strains – e.g., knock-out / knock-down mutants, complemented mutant strains, overexpressors - or from the functional complementation of defined E. coli mutants). In some cases, the function of a gene is exclusively based on its homology to other known (myco)bacterial genes. TMM, trehalose monomycolates; TDM, trehalose dimycolates.

^*Glycogen and methylglucose lipopolysaccharides were included in the analysis because they share common biosynthetic genes with capsular α-glucan. They are, however, cytosolic (lipo)polysaccharides.