OUR SCIENCE
In simpler terms, scientists usually study how genes affect the length of life and the aging process. They look at genes that can make you live longer or age faster.
One gene called bmk-1 is known to help with how cells divide, similar to its human version, KIF11. But, no one thought it had anything to do with aging until now.
We discovered that this bmk-1 gene actually plays a role in how long a tiny worm lives. When we reduce the activity of this gene in the worm, its lifespan gets shorter by 32%. But when we make the gene work more, the worm lives 25% longer and becomes better at handling heat stress. This gene seems to do this by changing the levels of certain proteins in the worm's cells.
One of these proteins, hsp-16, seems to be really important for making the worm live longer when bmk-1 is super active. It's like hsp-16 helps protect the cells from stress and prevents a process called apoptosis, which is like programmed cell death. All of this makes the worm live longer.
We're still not entirely sure if the gene does these things because it's good at cell division or if it has a new job related to aging. But what we do know is that bmk-1 could be a new target for helping animals, and even people, live longer and stay healthier as they age.
BREAKTHROUGH INNOVATIONS
Elevating lifespan by
an astonishing 25%
Figure 1. Bmk-1 over-expression extends lifespan and bmk-1 inhibition by RNAi shortens lifespan in C. elegans
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(A) qRT-PCR validation of bmk-1 over-expression worm lines shows increased bmk-1 gene expression (* indicates p < 0.01). Y-axis represents the relative expression level of bmk-1 normalized to act-1, and n ≥ 10 for each group.
(B) lifespan measurement for both WT (GFP-expressing, n = 126) and bmk-1 over-expressing (n = 161) animals. Both median lifespan and maximum lifespan of bmk-1 over-expressing lines show a 25% extension when compared to WT lines (p < 0.001, pvalues were derived from student t-test and log-rank test).
(C) qRT-PCR validated the RNAi effect, indicating a significant reduction (∼64%) of bmk-1 transcripts in WT worms treated with bmk-1 RNAi. Y-axis represents the relative expression level of bmk-1 normalized to act-1, and n ≥ 10 for each group. * indicates p < 0.01.
(D) A shortened lifespan, both median (32%) and maximum (15%), was induced by bmk-1-specific RNAi in C. elegans (n = 82), as compared to RNAi vector lines (n = 75) (p < 0.0001).