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Cystathionine β-synthase (CBS) is a housekeeping enzyme that catalyzes the first step of the homocysteine to cysteine transsulfuration pathway. Homozygous deletion of the  Cbs  gene in mice causes severe hyperhomocysteinemia and reduces life span. Here, we examined a possible involvement of senescence, mitochondrial DNA, and telomeres in the reduced life span of  Cbs  −/−  mice. We found that senescence-related  p21 ,  Pai-1 ,  Mcp1 , and  Il-6  mRNAs were significantly upregulated (2–10-fold) in liver, while  p21  was upregulated in the brain of  Cbs  −/−  mice ( n  = 20) compared with control  Cbs  +/−  siblings ( n  = 20) in a sex- and age-dependent manner. Telomere length in blood ( n  = 80), liver ( n  = 40), and brain ( n  = 40) was not affected by the  Cbs  −/−  genotype, but varied with sex and/or age. Levels of mitochondrial DNA tended to be reduced in livers, but not brains and blood, of  Cbs  −/−  females ( n  = 20–40). The  Cbs  −/−  genotype significantly reduced  Tert  mRNA expression in brain, but not liver, in a sex- and age-dependent manner. Multiple regression analysis showed that the senescence-related liver (but not brain) mRNAs and liver (but not brain or blood) mitochondrial DNA were associated with the  Cbs  genotype. In contrast, telomere length in blood, brain, and liver was not associated with the  Cbs  genotype or hyperhomocysteinemia, but was associated with sex (in brain and liver) and age (in brain and blood). Taken together, these findings suggest that the changes in senescence marker expression and mtDNA levels, but not telomere shortening, could account for the reduced life span of  Cbs  −/−  mice.

The Cbs Locus Affects the Expression of Senescence Markers and mtDNA Copy Number, but not Telomere Dynamics in Mice