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We develope a theoretical framework, based on exclusion process, that ismotivated by a biological phenomenon called transcript slippage (TS). In thismodel a discrete lattice represents a DNA strand while each of the particlesthat hop on it unidirectionally, from site to site, represents a RNA polymerase(RNAP). While walking like a molecular motor along a DNA track in astep-by-step manner, a RNAP simultaneously synthesizes a RNA chain; in eachforward step it elongates the nascent RNA molecule by one unit, using the DNAtrack also as the template. At some special "slippery" position on the DNA,which we represent as a defect on the lattice, a RNAP can lose its grip on thenascent RNA and the latter's consequent slippage results in a final productthat is either longer or shorter than the corresponding DNA template. Wedevelope an exclusion model for RNAP traffic where the kinetics of the systemat the defect site captures key features of TS events. We demonstrate theinterplay of the crowding of RNAPs and TS. A RNAP has to wait at the defectsite for longer period in a more congested RNAP traffic, thereby increasing thelikelihood of its suffering a larger number of TS events. The qualitativetrends of some of our results for a simple special case of our model areconsistent with experimental observations. The general theoretical frameworkpresented here will be useful for guiding future experimental queries and foranalysis of the experimental data with more detailed versions of the samemodel.

A Biologically Motivated Asymmetric Exclusion Process: interplay of congestion in RNA polymerase traffic and slippage of nascent transcript