This thesis consists of work on the wis1 pathway: the analysis of some of the upstream components and the isolation and characterisation of genes that lie downstream of wis1. The mcs4, win1 and wis4 genes had already been shown to lie upstream of wis1. Strains were constructed with different combinations of mutations in these genes. fbp1 transcription was assayed in these strains. An additive effect was seen in win1 wis4 double mutants, suggesting that win1 and wis4 act in parallel. To identify functionally-related genes downstream of wis1, the stress sensitivity of wis1Δ cells was exploited. A screen for extragenic suppressing mutations was carried out. Several hundred heat resistant mutants were isolated. Some also presented the salt sensitivity and/or cell length defect of wisΔ. Twelve such sow (for suppressor of wis1Δ) mutants, each of which containing a single suppressing mutation, were analysed further. They fell into two linkage groups: sow1 (nine strains) and sow2 (three strains). When the sow mutations were crossed into a wis1⁺ background, both sow1 and sow2 were able to grow at temperatures above the usual range for S. pombe. In addition, sow1 strains divide at a shorter length than wild type, indicating a mitotic advance, and sow2 cells have a slightly aberrant morphology. To determine whether the sow mutations corresponded to any known genes, crosses were carried out between the sow mutants and mutants in the following genes: wis1 pathway genes (sty1, atf1, ppa1, ppa2 and ppe1), cAMP pathway genes (cyr1, pka1) cell cycle regulation genes (cdc2, cdc25, wee1, cdc13), a heat shock protein (hsp90) gene (swo1) and a gene required for maintenance of the mitotic cell cycle (pat1).