Living systems have a remarkable ability to buffer against a multitude of perturbations and continually produce invariant phenotypes, known as robustness. One example of developmental robustness relates to cell fate patterning in C. elegans, which is so consistent that these animals are generally considered eutelic. We focus on the bilaterally present epithelial stem cell populations in C. elegans, the so-called seam cells, to identify factors that influence cell number variance using unbiased forward genetic approaches. In wild type, animals hatch with 10 seam cells on either lateral side and have a very invariant terminal seam cell number of 16 by adulthood. We show here that mutations in
bus-19, which encodes a conserved transmembrane protein and
srf-3, which encodes a nucleotide sugar transporter, lead to increased variability in seam cell number. Consistent with previous reports, we find that both mutations lead to a more permeable and morphologically defective cuticle. We show that
srf-3 expression is highly specific to the daughter cell that maintains the seam cell fate potential following the asymmetric divisions, whereas
bus-19 is expressed more broadly in the seam and hypodermis. Using time-lapse imaging of seam cell divisions, we characterise the errors that increase seam cell number variability. These errors occur more often during the L3 and L4 stages and are mainly of two kinds: conversion of asymmetric stem cell divisions to symmetric with both cell daughters either differentiating to hypodermis or retaining the seam cell fate, thus leading to a reduction or increase in terminal seam cell number respectively. We also see a large number of other patterning errors that do not modify the terminal seam cell number. These results identify a new link between seam cell patterning and cuticle integrity.