Male reproductive physiology - Meiosis and Mitosis

Basic Processes

Somatic cells replicate by mitosis, in which genetically identical daughter cells are formed. Germ cells replicate by meiosis, in which the genetic material is halved to allow for reproduction. Meiosis and sexual reproduction generate genetic diversity, providing a richer source of material on which natural selection can act. The life of a cell is divided into cycles, each of which is associated with different activities. About 5-10% of the cell cycle is spent in the mitotic phase (M), in which DNA and cellular division occurs. Cell replication by mitosis is a precise, well-orchestrated sequence of events involving duplication of the genetic material (chromosomes), breakdown of the nuclear envelope, and equal division of the chromosomes and cytoplasm into 2 daughter cells (

Table 42-2). The essential difference between mitotic and meiotic replication is that a single DNA duplication step is followed by only 1 cell division in mitosis, but 2 cell divisions in meiosis (4 daughter cells). As a consequence, daughter cells contain only half of the chromosome content of the parent cell. Thus, a diploid (2n) parent cell becomes a haploid (n) gamete. Figure 42-3 illustrates how the DNA content of the dividing cell changes with mitosis and meiosis. Other major differences between mitosis and meiosis are outlined in

Table 42-3.

Making Sperm

The mature spermatozoan is an elaborate, specialized cell produced in massive quantity, up to 300 per g of testis per second. Type B spermatogonia divide mitotically to produce diploid primary spermatocytes (2n), which then duplicate their DNA during interphase. After the first meiotic division, each daughter cell contains one partner of the homologous chromosome pair, and they are called secondary spermatocytes (2n). These cells rapidly enter the second meiotic division in which the chromatids then separate at the centromere to yield haploid early round spermatids (n). Thus, each primary spermatocyte theoretically yields 4 spermatids, although fewer actually result, as the complexity of meiosis is associated with germ cell loss.

The process by which spermatids become mature spermatozoa within the Sertoli cell can take several weeks and consists of several events:

1. The acrosome is formed from the Golgi apparatus.
2. A flagellum is constructed from the centriole.
3. Mitochondria reorganize around the midpiece.
4. The nucleus is compacted to about 10% of its former size.
5. Residual cell cytoplasm is eliminated.

The nucleus of the round spermatid is spherical but the shape changes from spherical to asymmetric as chromatin condenses. It is theorized that many cellular elements contribute to the reshaping process, including chromosome structure, associated chromosomal proteins, the perinuclear cytoskeletal theca layer, the manchette of microtubules in the nucleus, subacrosomal actin, and Sertoli cell interactions.

With completion of spermatid elongation, the Sertoli cell cytoplasm retracts around the developing sperm, stripping it of all unnecessary cytoplasm and extruding it into the tubule lumen. The mature sperm has remarkably little cytoplasm.

Sperm Maturation: The Epididymis

Spermatozoa within the testis have very poor or no motility and are incapable of fertilizing an egg. They become functional only after traversing the epididymis and the additional maturation process that it entails. Anatomically, the epididymis is classically divided into 3 regions: caput or head, corpus or body, and cauda or tail. Passage through the epididymis induces many changes to the newly formed sperm, including alterations in net surface charge, membrane protein composition, immunoreactivity, phospholipid and fatty acid content, and adenylate cyclase activity. These changes are thought to improve the membrane structural integrity and increase fertilization ability. The transit time of sperm through the fine tubules of the epididymis is thought to be 10-15 days in humans.

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Provided by ArmMed Media
Revision date: June 11, 2011
Last revised: by Dave R. Roger, M.D.