Why do sperm have tails

This effect is reminiscent of a human male sterility condition known as the "easily decapitated spermatozoa defect'. Semen from individuals affected by this condition appears normal, but minimal micro-manipulation, such as that required for in vitro fertilisation, results in sperm heads that are separated from their tails and thus that cannot swim. Primary cilia are a shorter version of flagella that are present in certain neurons in the fly and in many cell types in humans, where they function as sensors of external stimuli.

Like flagella, primary cilia contain a microtubule array that is templated by the basal body. Note: Content may be edited for style and length. Science News. A human condition: "easily decapitated spermatozoa defect' In addition to the faulty microtubule array within the tail, the head-to-tail link is often severed in CENTROBIN mutant sperm.

Centrobin is essential for C-tubule assembly and flagellum development inDrosophila melanogasterspermatogenesis. Become one now. To celebrate our centennial, we have made our entire archive available for free. But quality journalism comes at a price. Support the next century of science journalism. Skip to content. Science News Needs You Support nonprofit journalism.

Lee July 31, at pm. There was a problem signing you up. Microbes Are viruses alive, not alive or something in between? And why does it matter? By Megan Scudellari November 1, Glycolysis has been suggested to act as a spatial ATP buffering system, transferring energy ATP synthesized by respiration in the mitochondria located in the basal part of the flagellum to the distal part. By contrast, inhibition of glycolysis by alpha-chlorohydrine caused a significant decrease in the bend angle of the flagellar bending wave, sliding velocity of outer doublet microtubules and ATP content even in the presence of OXPHOS substrates [ ].

Several mouse models have established the importance of glycolysis and OXPHOS for sperm tail motility, although even with compromised motility the male mice are fertile. It appears that different energy metabolic pathways can, at least to some extent, compensate for variations in substrate supply. In addition to energy production, the hyperactivation of sperm motility in the female reproductive tract is pivotal for fertility.

The CatSper channels appear to be the main regulator of the calcium signaling and therefore hypermotility in sperm across species. Sperm encounters complex chemical and physiological barriers on the way to fertilize the oocyte. In order to overcome these obstacles, sperm must sense the environmental cues and change its swimming pattern, which is achieved by ion channels.

Recent studies have underlined additional ion channels, which regulate CatSper activity and are important for physiological conditions in mature sperm [ 65 , ]. Specific ion channels in the mid piece have also been identified e. However, the specific ion channels differ between species and thus require further studies to establish their importance and exact roles.

Although the morphological changes in sperm structure and motility defects prior to capacitation are easily visible, there are various factors influencing male fertility that can be detected only by specific biomarkers.

Identification of these mechanisms enables development of fertility-related diagnostics and therapeutics. It can be hypothesized that addition of different substrates in the environment of the sperm could improve the motility in presence of specific mutations.

On the other hand, the specificity of CatSper channels to sperm makes them an intriguing target for development of contraceptives [ 66 , ]. It is well known that sperm tail malformations and motility defects cause male infertility.

However, the underlining cause for the defects is often unknown. Human male infertility has been associated with several mutations in sperm tail accessory structures in addition to PCD. Furthermore, although the axonemal structure in cilia and sperm tail flagella is similar, it is becoming evident that differences in formation and function exist [ ].

In many PCD cases, male infertility is reported, but the sperm tail phenotype has not been investigated. Mutations in Dnah1 gene appear to be the most common identified cause for male infertility related to sperm tail formation [ — ]. Dnah1 has also been associated with PCD [ , ], but based on the current knowledge it is not crucial for dynein arm formation in cilia.

DnaJ homolog subfamily B member 13 DNAJB13 causes depletion of the axonemal central pair in motile cilia [ ], but has been transiently localized to the annulus in sperm tail [ ]. Mutation in a male patient also resulted in infertility, but the exact effect on sperm tail structure is not known [ ].

Furthermore, the importance of nonstructural proteins for sperm tail development has been recently recognized. Although the structural proteins have been studied and many are known, the events prior to structural assembly are poorly understood. Furthermore, mutations affecting the capacitation and hyperactivation of sperm, such as the CATSPER1 and CATSPER2 genes coding for CatSper subunits, have been identified in infertile male patients [ , ] and other genes affecting the same pathway are good candidates for infertility screening.

In addition to structural proteins, human male fertility also relies on proteins in preassembly and transport pathways prior to structural assembly and in storage and enzymatic pathways in mature sperm. The heterogeneity of male infertility substantially hampers identification of causal genes, but clear phenotype and recent advancements in sequencing technologies enable also identification of genetic causes of male infertility.

For resolving male factor infertility, it is crucial to identify and understand the factors and mechanisms contributing to fertile sperm. The identified genes affecting sperm motility can be used as biomarkers for male fertility.

For example, the known gene mutations causing PCD and sperm tail phenotype can be utilized for prediction of male infertility. The counseling of PCD patients for their fertility status is an important factor, and therefore the effect of identified PCD genes on male fertility should be studied.

Thus far, the effect has been poorly reported and therefore the usability of PCD genes as biomarkers also for male fertility is inadequate. Sperm-specific defects can be expected to rise from gene mutations affecting sperm tail accessory structures and motility pathways.

However, very limited number of mutations have been identified in human patients [ 17 , ], which indicates that additional studies are needed. However, the expression levels of known genes in sperm tail structures can be used as an indicator of fertility potential and these genes are good candidates for causative mutations. It is crucial to underline the roles of proteins in different tail structures for prediction of impact on fertilizing potential and developing embryo.

Although ICSI can be used for fertilization of the oocyte in vitro, the effects of sperm tail malformations on offspring are not well understood. Thus, it would be beneficial to introduce as natural conditions for in vitro fertilization IVF as possible. In the case of reduced motility, some energy supplements could be developed to increase motility in vitro. This ensures some level of natural selection for the offspring.

Furthermore, the recent development in genome editing methods and RNA therapeutics underline intriguing prospects on genetic correction of inherited mutations.

Genome editing involves major ethical issues, which need to be solved prior to therapeutic use. However, RNA therapeutics give promise for more short-term development of male infertility treatments.

Research is underway for new genetic therapeutics and diagnostics for genetic diseases and is an exciting field for treatment of male infertility as well. Sperm tail formation is a unique process, although the axoneme structure and protein transport mechanisms resemble motile cilia.

The results from various studies denote the importance of specific proteins for sperm tail basal body, HTCA, and axoneme formation. Due to the specialized long flagellum and required wave form for motility, the axoneme alone is not sufficient to provide the necessary rigidity and energy for sperm in order to reach and fertilize the oocyte.

The first phase required for formation of motile sperm after protein expression is the preassembly of required sperm tail components and transport to the assembly site. Thus far, studies have concentrated on the structural composition of the sperm tail structures; however, recent studies have indicated that regulation and transport prior to structural assembly are important factors in producing fertile sperm. These mechanisms are poorly studied and should be addressed in future investigations.

Since the role of the sperm tail is to produce motility, it is reasonable to conclude that mutations affecting any part of the sperm tail result in motility defects including biochemical properties required for capacitation and hypermotility. This hypothesis has been proven by previous studies, but additional investigations are needed for identification of the exact roles of axonemal and accessory structure proteins, differences between cilia and sperm tail, and the role of nonstructural proteins in order to decipher the genetic causes of male infertility.

Mutations in genes affecting specific structures of the sperm tail result in common phenotypes Figure 2 , Table 1 , which can be used in investigation of the cause of infertility. Although IVF and ICSI can overcome the lack of sperm motility, specific structural defects such as centrosome and axoneme malformation may influence the outcome of these technologies.

Thus, the understanding of the effects of genomic mutations and development of genetic therapeutics and diagnostics are of great importance. KO mouse models affecting the formation of sperm tail accessory structure. Axonemal defects have been recently reviewed in [ 17 ].

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