For all these reasons, it appears likely that several of the mutations specific to ‘PCC-M’ or shared with ‘PCC-P’ and ‘PCC-N’ may be related to the known phenotypes of these strains. For example, the truncation of sll1951 (haemolysin) and possible truncation of slr1753 (surface protein) may contribute to a stress-induced clumping phenotype. Several other mutations might cause alterations in glucose tolerance or phototactic behaviour of these substrains. Differences at other loci may affect the phage resistance, stress response or functions in the primary metabolism, potentially relevant for the synthesis of alkanes or the N and C metabolism. The absence of ISY203g in the sll1473–5 regions in PCC substrains leads to an intact photoreceptor that regulates the expression of an alternative phycobilisome linker gene.53 Regarding phenotypic differences among motile PCC substrains, it might be noteworthy that ‘PCC-M’, despite its general ability to be motile, is not phototactic towards blue light (see direct comparison of strains in Fig. 1 of Fiedler et al.48). Here, the SNP #39 in the sigF gene, known to be involved in the control of phototactic movement30 might be considered, as the resulting M231K substitution could influence the DNA–protein interaction of this group 3 sigma factor in a very subtle way. For sure, the subtle differences in genome sequences have to be considered when choosing a particular substrain for certain experiments and when comparing phenotypes of mutant lines from different laboratories with the wild-type strain. Information on the re-sequenced genome and plasmid sequences including precisely annotated SNPs can be found in the eight sequence files available from GenBank under the accession numbers CP003265–CP003272.