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• W2039448043 abstract "β-TrCP, the substrate recognition subunit of a Skp1–Cul1–F-box (SCF) ubiquitin ligase, is ubiquitously expressed from two distinct paralogs, targeting many regulatory proteins for proteasomal degradation. We generated inducible β-TrCP hypomorphic mice and found that they are surprisingly healthy, yet have a severe testicular defect. We show that the two β-TrCP paralogs have a nonredundant role in spermatogenesis. The testicular defect is tightly associated with cell adhesion failure within the seminiferous tubules and is fully reversible upon β-TrCP restoration. Remarkably, testicular depletion of a single β-TrCP substrate, Snail1, rescued the adhesion defect and restored spermatogenesis. Our studies highlight an unexpected functional reserve of this central E3, as well as a bottleneck in a specific tissue: a single substrate whose stabilization is incompatible with testicular differentiation." @default.
• W2039448043 created "2016-06-24" @default.
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• W2039448043 date "2010-03-01" @default.
• W2039448043 modified "2023-10-17" @default.
• W2039448043 title "Spermatogenesis rescue in a mouse deficient for the ubiquitin ligase SCF^β-TrCP by single substrate depletion" @default.
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• W2039448043 doi "https://doi.org/10.1101/gad.551610" @default.
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