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2016 ; 7
(39
): 64203-64220
Nephropedia Template TP
gab.com Text
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English Wikipedia
F5-peptide induces aspermatogenesis by disrupting organization of actin- and
microtubule-based cytoskeletons in the testis
#MMPMID27611949
Gao Y
; Mruk DD
; Lui WY
; Lee WM
; Cheng CY
Oncotarget
2016[Sep]; 7
(39
): 64203-64220
PMID27611949
show ga
During the release of sperm at spermiation, a biologically active F5-peptide,
which can disrupt the Sertoli cell tight junction (TJ) permeability barrier, is
produced at the site of the degenerating apical ES (ectoplasmic specialization).
This peptide coordinates the events of spermiation and blood-testis barrier (BTB)
remodeling at stage VIII of the epithelial cycle, creating a local apical ES-BTB
axis to coordinate cellular events across the epithelium. The mechanism(s) by
which F5-peptide perturbs BTB restructuring, and its involvement in apical ES
dynamics remain unknown. F5-peptide, besides perturbing BTB integrity, was shown
to induce germ cell release from the epithelium following its efficient in vivo
overexpression in the testis. Overexpression of F5-peptide caused disorganization
of actin- and microtubule (MT)-based cytoskeletons, mediated by altering the
spatiotemporal expression of actin binding/regulatory proteins in the
seminiferous epithelium. F5-peptide perturbed the ability of actin microfilaments
and/or MTs from converting between their bundled and unbundled/defragmented
configuration, thereby perturbing adhesion between spermatids and Sertoli cells.
Since apical ES and basal ES/BTB are interconnected through the underlying
cytoskeletal networks, this thus provides an efficient and novel mechanism to
coordinate different cellular events across the epithelium during spermatogenesis
through changes in the organization of actin microfilaments and MTs. These
findings also illustrate the potential of F5-peptide being a male contraceptive
peptide for men.