The cytosolic aldehyde dehydrogenase gene (Aldh1) is developmentally expressed in Leydig cells

Retinoic Acid Metabolism and Signaling Pathways in the Adult and Developing Mouse Testis

“…Thus, its high level of expression may permit conversion of retinaldehyde into RA in Leydig cells (Ref. 18 and present report). That Aldh1a1-null mutants do not display reproductive defects possibly reflects the existence of a functional compensation by RALDH3, which is detected at low levels in Leydig cells.…”

“…The first step, oxidation of ROL into retinaldehyde, involves alcohol dehydrogenases, of which three are expressed in the mouse testis: the ubiquitous ADH3, ADH1 in Sertoli cells, and ADH4 in late spermatids (14,15). The second step, oxidation of retinaldehyde into RA, is catalyzed by four retinaldehyde dehydrogenases (RALDH1-4, encoded by the Aldh1a1 to Aldh1a3 and Aldh8a1 genes, respectively) (11,16), of which Aldh1a1 and Aldh1a2 are expressed in the rodent testis (17,18). Alternatively, RA can be produced from ␤-carotenes carried along into chylomicron remnants (19), through their conversion into retinaldehyde by the ␤-carotene 15,15Ј-monoxygenase, which is expressed in testis (reviewed in Ref.…”

CABS1 Is a Novel Calcium-Binding Protein Specifically Expressed in Elongate Spermatids of Mice1

“…As shown in Figure 2 and Table 1 [23][24][25][26][27][28][29][30][31][32][33][34][35][36], the testicular proteins identified by TOF-MS were categorized into three groups according to the pattern of the changes in the contents and using actin (spot no. 3) as an unchanged control: unchanged (I), temporarily increased (II), and temporarily SPERM-SPECIFIC CALCIUM-BINDING PROTEIN, CABS1 decreased (III) proteins.…”

Retinoic acid metabolism, signaling, and function in the adult testis

“…The mRNA localization pattern of three of the four ALDH enzymes capable of oxidizing retinaldehyde-Aldh1a1, Aldh1a2, and Aldh1a3-has been described for the developing and adult testis. Conflicting localization patterns have been published for Aldh1a1 because it was originally reported to be Leydig cell specific [28], yet more recent studies have also detected transcript in Sertoli cells [29], spermatogonia, spermatocytes, and spermatids [30]. Interestingly, global deletion of Aldh1a1 in mice results in no phenotypic abnormalities, indicating that this enzyme is dispensable for male fertility.…”