Notably, these mutants exhibited significant growth phenotypes in response to sub-lethal rapamycin concentrations, suggesting that they were all either potentially regulated by TORC1, or function upstream of TORC1. Interestingly, the different mutants displayed a wide BMS-354825 variety of responses to rapamycin. Interestingly, mks1D mutants showed decreased resistance to rapamycin, in contrast with an earlier report. However, on several occasions, particularly with strains that had been maintained on drug-free plates for several weeks, we have observed that mks1D strains show a tendency to revert to an increased rapamycin-resistance phenotype. Both results only further confirm the chemical genetic link between Mks1p and the TORC1. Finally, two of these proteins, Mks1p and Ksp1p, displayed a rapamycin-dependent mobility shift during SDS-PAGE, as has also been shown earlier, suggesting their phosphorylation in a TORC1-dependent manner. Collectively, these data demonstrate that Mks1p, Kap123p, Hef3p, Ksp1p and Uba4p each can directly associate with TORC1, and that their biological functions are likely regulated in a TORC1-dependent manner. Our purifications of the TORC1 identified proteins involved in different types of yeast filamentous growth that were associated as part of the complex. However, both the CEN.PK and S1278b yeast strains show robust nitrogen-dependent diploid pseudohyphal growth, but the CEN.PK strain does not show haploid invasive growth under any of the other conditions. Therefore, we next attempted to ascertain if the TORC1 pathway and/or any of the identified TORC1-associated proteins played a role in nitrogen-independent invasive growth. First, we tested invasive growth in haploid, prototrophic S1278b background yeast strains under a variety of conditions, in the presence or absence of sublethal concentrations of the TORC1 inhibitor rapamycin. Yeast BEZ235 continue to show robust invasive growth even under partial TORC1 inhibition by rapamycin, except when grown with ethanol as the sole carbon source. These data suggest that the TORC1 pathway may not significantly regulate haploid invasive growth. Consistent with this observation, most deletion mutants of proteins we identified as TORC1- associated continued to show significant invasive growth under these conditions. ksp1D deletion mutants showed slightly diminished invasive growth only under some invasive growth conditions. The data presented in this study provide insight into the broader roles of the TORC1 in response to low nitrogen levels. Our data show that the TORC1-interacting proteins identified in this study are involved in diploid pseudohyphal growth. Interestingly, these proteins show different responses to rapamycin treatment.