Remember that rRNA genes have a high copy number: around 200 in humans, and this number is not actually a massive surplus. Ribosomes are hugely important to cellular activity and replication, and the cell needs a lot of them. Under rapid proliferation (such as embryonic development, or epithelial turnover, or wound healing) you need that many copies of the rRNA gene, all loaded with RNA polymerases, all pumping out rRNAs as fast as they can, just to keep up with demand.

A mutation that leads to non-functional ribosomes will thus have a small (0.5%) affect on supply of ribosomal RNA, but is unlikely to be of significant biological consequence (indeed, what with copy number variation, it is likely that humans show greater variety in total rRNA genes than +/- 1).

In essence, consider rRNA mutations to be heavily 'buffered': you'd need a lot of mutations in a lot of genes to produce marked impact on ribosome activity.

Thank you John Hildyard! You addressed the matter in a comprehensive way. Still I need some explanation about the effects of CNVs on rRNA functions.

Irfan, Please let me know if you find the attached papers informative to the underlying basis of your question. This is an area of investigation that we are actively pursuing. I think our most recent papers on the subject open up the discussion a bit further than is afforded by the functional/non-functional paradigm.

Dear Blanchard

These articles are really amazing. I got more interested in the topic and anticipate for more wonderful results in the subject