Abstract <p>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 mostly to shortening and (less frequently) to lengthening of telomeres, which impairs their functionality. In humans, telomere attrition is linked to diseases. Beyond mutations, many stress factors contribute to alteration of telomere length (TL). Budding yeast, <i>Saccharomyces cerevisiae,</i> is a popular model for studying telomere biology. Thermal stress was one of the first among discovered extrinsic factors causing telomere shortening in budding yeast, a species with constitutive expression of telomerase. 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 <i>mre11</i>Δ mutants with very short telomeres do not generate Tmp^– phenotype while <i>pif1</i>Δ mutants possessing very long telomeres do generate it and reduce their TL to the level in wild type cells grown under normal conditions. The absence of Tmp^– phenotype itself could be a generic feature for phenotyping other mutants responding to heat in the same way. In addition, <i>mre11</i>Δ mutants exposed to elevated temperature manifested altered telomeric DNA patterns resembling those in type I survivors. These patterns are thought to result from recombinational processes within telomeric DNA. We discuss the relevance of our findings to fundamental and applied research.</p>