title: Absence of aryl hydrocarbon receptor alters CDC42 expression and prevents actin polymerization during capacitation.
abstract: The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that regulates the toxicity of a variety of environmental chemicals. The absence of this receptor causes serious reproductive complications. Ahr-knockout (Ahr-KO) male mice, for example, are considerably less fertile: Half of the few spermatozoa they produce exhibit morphological alterations, and those with typical morphology may have pathologic modifications. We therefore investigated the consequences of AHR loss on capacitation and the acrosome reaction, and asked if these effects are a consequence of changes to actin polymerization and the expression of Cdc42, which encodes Cell division control protein 42 (CDC42), a RHO protein that controls assembly of the actin cytoskeleton in somatic cells as well as during spermatogenesis. Nearly 50% of spermatozoa produced by Ahr-KO mice had alterations in the flagellum. Ahr-KO spermatozoa were frequently capacitated, but showed reduced spontaneous and progesterone-induced acrosome reaction-which is related to low CDC42 abundance and very limited actin polymerization during capacitation. Thus, the expression of CDC42 might be regulated by AHR, and both proteins are fundamental to the development of normal spermatozoa and the acrosome reaction. Mol. Reprod. Dev. 83: 1015-1026, 2016 © 2016 Wiley Periodicals, Inc.
authors.affiliation: Departamento de Biología Celular, CINVESTAV-IPN, Av. Instituto Politécnico Nacional 2508, CP 07360, México DF, México.
authors.forename: Tania
authors.initials: T
authors.lastname: Angeles-Floriano
authors.affiliation: Departamento de Biología Celular, CINVESTAV-IPN, Av. Instituto Politécnico Nacional 2508, CP 07360, México DF, México.
authors.forename: Ana L
authors.initials: AL
authors.lastname: Roa-Espitia
authors.affiliation: Facultad de Medicina y Cirugía, Universidad Autónoma Benito Juárez de Oaxaca, Oaxaca, Cátedras CONACYT.
authors.forename: Rafael
authors.initials: R
authors.lastname: Baltiérrez-Hoyos
authors.affiliation: Departamento de Biología Celular, CINVESTAV-IPN, Av. Instituto Politécnico Nacional 2508, CP 07360, México DF, México.
authors.forename: Joaquin
authors.initials: J
authors.lastname: Cordero-Martínez
authors.affiliation: Departamento de Biología Celular, CINVESTAV-IPN, Av. Instituto Politécnico Nacional 2508, CP 07360, México DF, México.
authors.forename: Guillermo
authors.initials: G
authors.lastname: Elizondo
authors.affiliation: Departamento de Biología Celular, CINVESTAV-IPN, Av. Instituto Politécnico Nacional 2508, CP 07360, México DF, México.
authors.forename: Enrique O
authors.initials: EO
authors.lastname: Hernández-González
mesh_terms: D008841:Actin Cytoskeleton / Q000235:genetics / Q000378:metabolism; D000199:Actins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D005786:Gene Expression Regulation; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D018336:Receptors, Aryl Hydrocarbon / Q000172:deficiency*; D013075:Sperm Capacitation; D013094:Spermatozoa / Q000378:metabolism*; D020764:cdc42 GTP-Binding Protein / Q000235:genetics / Q000378:metabolism*
chemical_list: D000199:Actins; C581598:Cdc42 protein, mouse; D018336:Receptors, Aryl Hydrocarbon; D020764:cdc42 GTP-Binding Protein