Anomalies of Centriolar Derivatives Manifest in Spermatic Flagella and Respiratory Cilia of the Stallion

Abstract

Anomalies of centriolar derivatives were identified in ejaculates and testicular and tracheal biopsies of a sterile stallion, using light, scanning, and transmission electron microscopy. LM revealed that over half the sperm population had only a vestigial or no tail, while the rest had tails of variable length and shape. The vestigial tail was represented by its anlage, which was implanted on the nucleus and differentiated up to capitulum and collum stage. The stunted tail had an axoneme and its derivatives, but was short in all tail segments. Regardless of the tail length or shape, virtually all axonemes were devoid of the central tubular complex ("9 + 0" defect). Abnormal tail segmentation was associated with missing or defective flagellar sheaths and a profusion of extraneous dense fibers, which contributed to the knobby, bulbous, or lobuliform tail configurations. The gradient of flagellar anomalies seems associated with the inability of the distal centriole to implant on the plasmalemma, to produce the axoneme, or maintain its growth, and to induce the normal differentiation of periaxonemal structures. In contrast to sperm, the tracheal epithelium displayed moderate changes, which are manifest in circumscribed rarefaction of cilia, increased incidence of compound cilia, and disturbed orientation of cilia regarding the plane of central tubular complex. The tracheal cilia were free of "9 + 0" defect.

Notulae seminologicae. 2. The ‘short tail’ and ‘stump’ defect in human spermatozoa

“…Only a few slightly longer tail stump present accessory fibres and 9 + 2 short axonemes. Subsequently immotile spermatozoa with several kinds of reduced tails were described in an infertile stallion (Hrudka et al, 1991). This defect was named 'short tail' defect.…”

A comparative overview of the sperm centriolar complex in mammals and birds: Variations on a theme

“…The most obvious manifestation of this form of centriolar defect is reflected in the "stump tail" or "short tail" sperm defect, the distinction being made in terms of the length of the flagellum in affected cells (Andersson et al, 2000). This defect has been described in various mammalian species (Andersson et al, 2000;Hrudka et al, 1991) and irrespective of the length of the stunted tail, a common feature is the disruption of the normal 9 x 2 + 2 arrangement of the axonemal microtubules, in particular the loss of one or both of the central singlet microtubules (Andersson et al, 2000;Hrudka etal., 1991). According to Hrudka et al (1991) this defect "seems associated with the inability of the DC to implant on the plasmalemma, to produce the axoneme, or maintain its growth, and to induce the normal differentiation of periaxonemal structures".…”

“…This defect has been described in various mammalian species (Andersson et al, 2000;Hrudka et al, 1991) and irrespective of the length of the stunted tail, a common feature is the disruption of the normal 9 x 2 + 2 arrangement of the axonemal microtubules, in particular the loss of one or both of the central singlet microtubules (Andersson et al, 2000;Hrudka etal., 1991). According to Hrudka et al (1991) this defect "seems associated with the inability of the DC to implant on the plasmalemma, to produce the axoneme, or maintain its growth, and to induce the normal differentiation of periaxonemal structures". Other syndromes in man that point towards defective functioning of the DC include primary ciliary diskinesia (PCD) and dysplasia of the fibrous sheath (DFS).…”

“…Whereas the range of anomalies associated with the CC has been grouped as a specific syndrome for human sperm (Chemes, 2000(Chemes, , 2012Chemes et al, 1999;Chemes and Sedo, 2012;Dadoune, 1988;Holstein et al, 1988;Moretti and Collodel, 2012;Sathananthan, 2012;Zamboni, 1992) less comprehensive or encompassing descriptions are available for other mammals (Andersson et al, 2000;Barth and Oko, 1989;Blom and Birch-Andersen, 1970;Brito, 2007;Hrudka et al, 1991;Oettlé and Soley, 1988). In birds, this syndrome has only been described in any detail in ratites Soley, 2011a,b,2012a,b; while studies on poultry are silent on the topic.…”

“…Moreover, an association between abnormal alignment of the headflagellum junction and poor centrosomal function has been established (Comizzoli and Wildt, 2012;Manandhar et al, 2005) which adversely affects fertilization or impairs development of the zygote (Moretti and Collodel, 2012). Additionally, failure of the DC to initiate a normal 14 axoneme also results in deficient sperm motility (Andersson et al, 2000;Hrudka et al, 1991).…”