Telomeres are DNA-protein complexes capping chromosomal ends to secure genomic integrity in all eukaryotes. Many genes are involved in telomere maintenance. Mutations in those genes lead to shortening and (rarely) to lengthening of telomeres that affect their functionality. In humans, telomere attrition is often linked to diseases. In addition to mutational events, many stress factors contribute to alteration of telomere length (TL). Budding yeast, Saccharomyces cerevisiae, is a very popular model species for studying telomere biology. Thermal stress was one of the first among discovered extrinsic factors causing telomere shortening. Temperature-induced decline in TL is known as Tmp - phenotype. This vivid phenomenon highlights possibilities to manipulate TL by exogenous factors. Here we show that mre11Δ mutants with very short telomeres do not generate Tmp - phenotype, while pif1Δ mutants possessing very long telomeres do generate it and reduce their TL to the level of TL in wild type (WT) cells grown under normal conditions. It was also observed that mre11Δ mutants exposed to elevated temperature (35 oC) altered their telomeric DNA patterns resembling those in type I survivors. These patterns are thought to result from recombinational processes within telomeric DNA. We discuss relevance of these findings to fundamental and applied research.