Abstract
If we’re lucky, we get old. Physical and mental decline are negative hallmark associations of aging. Imagine being born blind and, as you approach middle age, waking up with the ability to see. In this issue of PLOS Genetics, Cornils, Maurya, and colleagues discover such a phenomenon: age-related suppression of ciliogenesis defects [1].
Highlights
Cilia are microtubule-based organelles that protrude from most nondividing cells in the human body
Many of the genes required for the formation, specialization, and sensory properties of C. elegans cilia have human counterparts that, when mutated, cause ciliopathies [6,8,9]
Visualization of cilia with in vivo cell-specific reporters reveals Age-dependent ciliary recovery (AdCR) in multiple cilia types, suggesting that, with age, all cilia have the potential to recover from an inherited genetic insult
Summary
Cilia are microtubule-based organelles that protrude from most nondividing cells in the human body. In this issue of PLOS Genetics, Cornils, Maurya, and colleagues discover such a phenomenon: age-related suppression of ciliogenesis defects [1]. Anterograde kinesin-2 and retrograde dynein motors transport the multi-protein IFT-A and IFT-B complex machinery and associated cargo along the microtubule-based ciliary axoneme. In Chlamydomonas and C. elegans, mutations in the IFT motors or the IFT machinery result in flagella-less algae or cilia-less worms, respectively.
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