I am a little concerned about the conclusion that this chromosomes is linear. Such a conclusion is very important that it deserves better evidence. The supporting restriction-hybridization analysis (Fig. 2) is not clear to me as to how the sizes of these fragments support linearity. If the chromosome is linear, one of the NotI, BamH1 and BglII sites would be mapped together at the telomeres. Should the author not show the maps?

Furthermore, there are wrong and misleading statements in the last paragraph in the Section - Genome size and organization

The following statement is incorrect: 'Streptomyces coelicolor replicon ends are composed of single-stranded sequences that can anneal to form a noncovalent circular molecule [3].' Linear chromosomes and linear plasmids of Streptomyces (not just S. coelicolor) are capped by terminal proteins covalently bound to the 5' end of the DNA. The DNA molecules have blunt ends. Single-stranded 3' overhangs are formed when replication forks reach there and fail to replicate the very ends. There is no such thing as annealing of the single-stranded ends to form a circle.

The next statements propose a unique mechanism for protection of the K. radiotolerans telomeres. The first statement is not quite right. First of all, there is more than one families of terminal proteins that covalently bind Streptomyces telomeres. While there is a conserved family of TPs, there are also 'atypical' ones, such as Tpc that caps SCP1 plasmid (which is very different in sequence and size). Other atypical telomeres of Streptomyces chromosomes and plasmids are almost certainly capped by other kinds of TPs. Besides, among other TP-capped linear replicons, including those of viruses such as adenoviruses and phi-29 phage of Bacillus, there are big variations in aa sequences and sizes among different classes. If the K. radiotolerans linear replicons are also capped by TPs, there is no reason to believe that they would use homologs of Streptomyces TPs. Besides, the K. radiotolerans may have hairpined telomeres as Borrelia and Agrobacterium. In either case, such mechanisms of 'protection' would not be unique. Moreover, while the TPs may probably serve a protective function in vivo, their crucial role is acting as primer for DNA synthesis that patches the 3' single-stranded gaps during replication.