Moss Life Cycle
2.1 The egg is already an organised cell #
2.1.1 A meiosis that waits #
Oogenesis is meiosis plus growth, and the growth is extreme. Primordial germ cells colonise the gonad, proliferate as oogonia, and enter meiosis as primary oocytes. In mammals they arrest in diplotene of prophase I, the dictyate stage, before birth, and can sit there for decades. The first meiotic division is completed, in the usual mammalian and amphibian cycle, only as the oocyte ovulates. It throws off a tiny first polar body. The egg then arrests at metaphase II under cytostatic factor, and the second polar body is extruded only after fertilisation. Both divisions are asymmetric so that cytoplasm stays in the oocyte.
The long prophase arrest is why maternal age raises the chance of chromosome segregation errors. Cohesin that has held homologues together for years fails more often. The cohesin machinery itself is the cell-cycle material in Cell Biology. The developmental fact is simply that the egg’s meiosis is paused twice, and sperm unpause the second arrest.
Amphibian oocytes are also transcriptionally furious during diplotene. Lampbrush chromosomes, with hundreds of laterally looped transcription units, are the visible sign. Much of that RNA is for the oocyte’s own growth, including an enormous stock of ribosomes. A separate, developmentally decisive fraction is stored as localised maternal mRNA for the embryo.
2.1.2 What is stored, and where #
Yolk, mitochondria, ribosomes, tRNA, proteins, and mRNAs are stockpiled because the early embryo cannot yet feed and, in many species, cannot yet transcribe. Yolk distribution will decide cleavage geometry in Chapter 3. In amphibians, vitellogenin made in the mother’s liver is taken up by the oocyte and packed into platelets. Mammalian eggs store very little yolk. The embryo will implant and be supplied by the mother, so the egg can be small, about 100 Β΅m in the human, and cleavage can cut the whole cell.
Storage is spatial, not only quantitative. In Drosophila, bicoid mRNA is anchored at the anterior cortex and nanos mRNA at the posterior pole plasm. In Xenopus, VegT mRNA and Vg1 mRNA sit at the vegetal pole, and a dorsal-determining machinery is parked in the vegetal cortex ready to be moved at fertilisation. The unfertilised egg is not a blank sphere. It is a cell with an animalβvegetal axis already, and in the fly with both axes roughed in by the mother.
Mammalian oocytes grow inside follicles. The zona pellucida, a glycoprotein coat of ZP1, ZP2, and ZP3, is secreted around the egg, and cumulus cells surround that. The zona is where species recognition and the slow block to polyspermy will act. Endocrine control of the follicle is Animal and Human Physiology.
2.1.3 Maternal-effect genes #
A maternal-effect gene is transcribed from the mother’s genome, during oogenesis, and its product is put into the egg. The phenotype of the embryo therefore follows the mother’s genotype, not the embryo’s own. A mother homozygous for a loss-of-function mutation in bicoid produces eggs whose embryos lack head and thorax, even if the father contributes a wild-type allele. That allele is in the zygotic genome, and the zygotic genome is not yet being used for anterior pattern when Bicoid protein has to act.
This is the bridge from gametogenesis to patterning. Chapters 4 and 5 begin with asymmetries the mother loaded into the cytoplasm. Genetics owns the pedigree pattern: affected offspring come from mutant mothers, and a heterozygous mother is typically normal because she still loads wild-type product. These notes own the reason the pedigree looks like that. The father’s genome matters later, when zygotic transcription starts, and it matters immediately for the chromosomes themselves. It does not, on its own, replace a missing anterior morphogen that should already have been in the egg.
Maternal effect is not a fly curiosity. The direction of spiral cleavage in a snail, dextral or sinistral, is set by a maternal product acting on the egg cytoskeleton, and the shell later coils the same way. The offspring’s own genotype controls the coiling of its grandchildren’s generation, not its own shell. Same logic as bicoid: the relevant transcription happened in the mother.
2.2 Spermatogenesis in outline #
2.2.1 A genome delivered, not a cytoplasm #
Spermatogenesis has to do the opposite of oogenesis. It produces a motile, stripped cell. Spermatogonial stem cells divide in the testis; primary spermatocytes complete meiosis I, secondary spermatocytes complete meiosis II, and the resulting spermatids undergo spermiogenesis. The Golgi builds the acrosome. A centriole organises the flagellar axoneme. Mitochondria wrap the midpiece. Histones are replaced by protamines so the nucleus condenses. Excess cytoplasm is shed as a residual body. The finished sperm is transcriptionally silent.
The developmental consequence is asymmetry at fertilisation. The egg contributes nearly all the cytoplasm, the mitochondria in most animals, the stored mRNAs, and the membranes on which blocks to polyspermy will run. The sperm contributes a haploid genome, and in most animals a centriole that helps organise the zygotic aster. Rodents are an exception to the centriole contribution. Endocrine support of spermatogenesis, and the anatomy of the male tract, are Animal and Human Physiology. The point required here is only that two gametes do not enter the zygote as equals.
2.3 Fertilisation #
2.3.1 Getting through the coats #
Fertilisation is species-specific membrane fusion plus the start of development. The steps differ in detail between a sea urchin, which fertilises externally, and a mammal, which fertilises inside the female tract. The jobs are the same: recognise the right egg, cross the coats, fuse one sperm, and stop the rest.
In the sea urchin, contact with the egg jelly triggers the acrosome reaction. The acrosomal vesicle exocytoses, and actin polymerises to push out an acrosomal process. Bindin on that process binds a receptor on the vitelline envelope in a species-specific way. The jelly carbohydrates that trigger the reaction are themselves species-biased. Specificity is checked twice, once to start the acrosome reaction and once to bind.
In mammals the sperm must first be capacitated in the female tract: cholesterol and coating glycoproteins are reorganised, cAMP rises, tyrosine phosphorylation increases, and the flagellum becomes hyperactivated. Only then can the sperm undergo the acrosome reaction and fertilise. The sperm crosses the cumulus, binds the zona, and the acrosome reaction releases enzymes that help it through. The old textbook certainty that ZP3 is the single sperm receptor is no longer safe. What is safe is that zona glycoproteins carry species-specific binding, and that cleavage of ZP2 after fertilisation destroys the egg’s ability to bind sperm. Fusion of the two plasma membranes uses a defined pair: Izumo1 on the sperm and Juno on the egg. Without either protein, membranes do not fuse.
2.3.2 Two blocks to polyspermy #
One sperm is the normal requirement in sea urchins, frogs, and mammals. Extra sperm bring extra centrosomes. Extra centrosomes make multipolar spindles, the chromosomes mis-segregate, and the embryo dies. Some animals, including birds, many insects, and urodele amphibians, are physiologically polyspermic: several sperm enter, and all but one male nucleus are later destroyed. The blocks below are the story for the groups that cannot tolerate extras. They are not a universal law of eggs.
The fast block is electrical. In the sea urchin, sperm fusion depolarises the egg membrane from a negative resting potential to a positive fertilisation potential, about +20 mV. Further sperm cannot fuse with a positive membrane. The block is immediate and temporary. It holds the fort for about a minute. Frogs have a comparable electrical block. Mammals do not use one.
The slow block is the cortical reaction, and it is permanent on the time scale of fertilisation. Cortical granules fuse with the egg membrane and release their contents. In the sea urchin, enzymes clip sperm receptors on the vitelline envelope, the envelope is cross-linked and lifted off as the fertilisation envelope, and hyalin builds a layer to which blastomeres will stick. In mammals, cortical-granule ovastacin cleaves ZP2, sperm binding sites are lost, and the zona hardens. This is the zona reaction. Mammals also change the egg membrane itself so that fusion fails even if a sperm reaches it. Juno is shed from the membrane after fertilisation, which removes the Izumo1 partner from the egg surface. The fast electrical block, where it exists, is a stopgap. The cortical reaction is the lock.
2.3.3 Calcium, activation, and the pronuclei #
Sperm entry opens development by a rise in cytosolic free calcium, released from the endoplasmic reticulum through IP3-gated channels. Cell Biology covers IP3 as a second messenger. The developmental pattern of the rise is not the same in every animal. In the sea urchin a wave starts at the point of sperm entry and crosses the egg within seconds, and it is enough to fire the cortical granules and activate metabolism. In mammals, a sperm-delivered phospholipase C, PLC-ΞΆ, generates IP3 inside the egg and the calcium rises repeatedly, as oscillations lasting hours. A single pulse does not fully activate a mammalian egg. Oscillations are part of the signal, not noise.
Calcium does three jobs at once. It triggers the cortical reaction. It restarts metabolism and the cell cycle. And it lets meiosis finish. Metaphase II arrest is held by cytostatic factor, including the Mos kinase pathway and the APC/C inhibitor Emi2, which together keep cyclin B and MPF activity high. The calcium rise activates CaMKII, Emi2 is degraded, the APC/C is freed, cyclin B and securin are destroyed, and the egg exits metaphase. The spindle, the APC/C, and CDK1 are Cell Biology. The developmental statement is that sperm entry is read as a calcium code that lifts a deliberate arrest.
Pronuclear union is also not one universal picture. In the sea urchin the sperm nucleus decondenses, the two pronuclei migrate, and they fuse into one diploid zygote nucleus. In mammals the two pronuclei approach, replicate their DNA while still separate, and their envelopes break down only as the first mitosis starts. The chromosome sets meet on a common spindle. There is no single fused interphase nucleus before cleavage. Maternal histones replace sperm protamines as the male chromatin opens. Calling both events “fusion of pronuclei” hides a real difference in when diploidy is first housed in one nucleus.
2.4 Key terms, summary, and self-check #
Key terms. Dictyate arrest; maternal mRNA; maternal-effect gene; acrosome reaction; capacitation; bindin; Izumo1; Juno; fast block; cortical reaction; zona reaction; PLC-ΞΆ; cytostatic factor; pronucleus.
Summary. The egg arrests meiosis, stockpiles cytoplasm, and localises maternal products that will pattern the embryo before the zygotic genome is in charge. The sperm delivers a genome and, usually, a centriole. Fertilisation checks species identity, admits one sperm by a temporary electrical block in some animals and a permanent cortical reaction in general, and uses calcium to restart the cell cycle. A maternal-effect gene mutates the mother’s contribution to that cytoplasm, which is why the father’s wild-type allele can arrive too late.
Self-check.
1. Why does a wild-type bicoid allele from the father fail to rescue embryos of a homozygous bicoid mutant mother?
2. What does membrane depolarisation achieve in a sea-urchin egg, and why is that not the mammalian block to polyspermy?
3. Which zona protein is cleaved by a cortical-granule enzyme, and what binding event does that cleavage stop?
4. Why are calcium oscillations, rather than one transient, required in the mammal, and which sperm protein starts them?
5. In what structural sense do mammalian pronuclei “not fuse” before the first cleavage?
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