Recently discovered simple quantitative relations knowns as bacterial growth laws hints on the existence of simple underlying principles at the heart of bacterial growth. In this work we provide a unifying picture on how these known relations, as well as new relations which we derive, stems from a universal autocatalytic network common to all bacteria, facilitating balanced exponential growth of individual cells. We show that the core of the cellular autocatalytic network is the transcription-translation machinery which by itself is an autocatalytic network composed of several coupled autocatalytic cycles like ribosome, RNA-polymerase and tRNA charging cycles. We derive two kinds of growth laws per autocatalytic cycle,  relating growth rate to the relative fraction of the catalyst and its catalysis rate and relating growth rate to all the time-scales in the cycle. The autocatalytic network structure defines multiple growth regimes , determined by the limiting components . The number of growth regimes can be very large , while the number of growth laws obtained can be much smaller. We  derive a growth law that accounts for RNA-polymerase auto-catalytic cycle, which we use to explain the dependence of growth rate on an inducible expression of  rpoB and rpoC genes that code for RpoB and RpoC protein subunits of RNA-polymerase, and to explain how the concentration of rifampicin -- a drug that targets RNA-polymerase , affects growth rate without changing the RNA to protein ratio. We further derive growth laws for tRNA synthesis and charging  and predict how perturbations to ribosome assembly or membrane synthesisaffect the growth rate .
Recently discovered simple quantitative relations known as bacterial growth laws hints on the existence of simple underlying principles at the heart of bacterial growth. In this work we provide a unifying picture on how these known relations, as well as new relations which we derive, stems from a universal autocatalytic network common to all bacteria, facilitating balanced exponential growth of individual cells. We show that the core of the cellular autocatalytic network is the transcription--translation machinery -- in itself an autocatalytic network comprising several coupled autocatalytic cycles , including the ribosome, RNA polymerase, and tRNA charging cycles. We derive two types of growth laws per autocatalytic cycle, one relating growth rate to the relative fraction of the catalyst and its catalysis rate , and the other relating growth rate to all the time--scales in the cycle. The structure of the autocatalytic network generates numerous regimes in state space , determined by the limiting components , while the number of growth laws can be much smaller. We also derive a growth law that accounts for the RNA polymerase autocatalytic cycle, which we use to explain how growth rate depends on the inducible expression of the rpoB and rpoC genes , which code for the RpoB and RpoC protein subunits of RNA polymerase, and how the concentration of rifampicin , which targets RNA polymerase , affects growth rate without changing the RNA-to-protein ratio. We derive growth laws for tRNA synthesis and charging , and predict how growth rate depends on temperature, perturbation to ribosome assembly and membrane synthesis .
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