The rate of cell growth is directly dependent on the rate of protein synthesis, which is itself intricately linked to ribosome synthesis and rRNA transcription. Thus, intracellular signals must coordinate the synthesis of rRNA with that of other components of protein translation. Myc is known to bind to human ribosomal DNA in order to stimulate rRNA transcription by RNA polymerase I.  Two specific mechanisms have been identified, ensuring proper control of rRNA synthesis and Pol I-mediated transcription.
Given the large numbers of rDNA genes (several hundreds) available for transcription, the first mechanism involves adjustments in the number of genes being transcribed at a specific time. In mammalian cells, the number of active rDNA genes varies between cell types and level of differentiation. In general, as a cell becomes more differentiated, it requires less growth and, therefore, will have a decrease in rRNA synthesis and a decrease in rDNA genes being transcribed. When rRNA synthesis is stimulated, SL1 (selectivity factor 1) will bind to the promoters of rDNA genes that were previously silent, and recruit a pre-initiation complex to which Pol I will bind and start transcription of rRNA.
Changes in rRNA transcription can also occur via changes in the rate of transcription. While the exact mechanism through which Pol I increases its rate of transcription is as yet unknown, evidence has shown that rRNA synthesis can increase or decrease without changes in the number of actively transcribed rDNA.