This one big cell is the fertilized oocyte.

This one big cell then divides
very rapidly, in the embryos of most kinds of animals
But not in the embryos of mammals, including humans; our early embryos divide only about once per day; cell cycle times of 20 hours are normal for many tissues in the body, and for tissue culture cells.

Each of these rapid divisions are called "cleavage".
For example, in sea urchin embryos the time between divisions is an hour to a half-hour.
Fly embryos have cell cycle times as short as ten minutes

These cleavage divisions produce several hundreds or thousands of cells
(this depends on the species; more in some species, fewer in others)

The cleavage divisions create the blastula stage of development.

The cells of the blastula then actively rearrange in gastrulation.

This creates the body axis and digestive tract.
(although this axis has often been decided on long before)

Cell differentiation begins during and after gastrulation.
Then organs are formed, in "organogenesis"

Several important kinds of differences in these cleavage divisions

Whether the usual controls on the cell cycle are temporarily turned off.

(These control mechanisms are turned off in frog embryos
but ARE not turned off in mammal embryos)

For example, the mechanism that prevent DNA synthesis from beginning (the S period) until it has checked whether DNA is damaged.

Another example of a checkpoint is the mechanism that prevents mitosis from beginning until it checks that DNA synthesis has been completed.

Because these checkpoint mechanisms have been turned off,
frog embryos have no G1 and G2 periods during cleavage.

Their cell cycle is just M-S-M-S-M-S-M-S-M-S-M-S-M-S-M-S
Until the blastula stage, when these control checkpoints are reactivated,
so the cycle becomes M-G1-S-G2-M-G1-S-G2-M-G1
(as it is ordinary cells).

The time when these checkpoints again become active, so that the cells again have G1 and G2 periods, has been named the"mid-blastula transition".
It is also often the time when transcription of m-RNA increases.

This is also related to the cleavages being synchronous
(meaning that all cells divide at the same time) although I don't really understand why.
(The book implies a causal connection between synchrony and the lack of checkpoints, but it doesn't say why lack of checkpoints should cause simultaneous division)

Mammals are very odd in these respects: we do NOT turn off
the cell cycle checkpoints, our early embryonic cells
do not cleave synchronously, cleave slowly (20+ hour cell cycle)
and these cells continue to have G1 and G2 periods.

Looking ahead to future subjects, it turns out that most cancers are caused by failure of these same checkpoint controls on the cell cycle, so cells are allowed to grow and divide without normal control!
(but cancer cells usually don't grow faster than normal)

Even more surprising, and interesting is that the reason why most cancer chemotherapy kills more cancer cells than normal cells is NOT because of differences in growth rates, but probably because functioning checkpoints serve to protect normal cells against damage, (but cancer cells are not protected). This is one of the reasons that these embryological phenomena are medically important)

Other differences between cleavage in different species:

Holoblastic cleavage in contrast to meroblastic cleavage
(whether the egg cell cleaves all the way through (as in amphibian eggs, sea urchin eggs and human eggs), in contrast to what happens in bird, reptile and teleost fish eggs, where only a surface layer of cytoplasm cleaves, and the yolky parts do not cleave)

Radial cleavage in contrast to spiral cleavage
(radial and spiral are both special kinds of holoblastic cleavage)
Sea urchins and amphibian eggs have radial cleavage; for example in the third cleavage (4 cells-> 8 cells), the 4 cells near the animal pole are each directly over one of the 4 vegetal cells.
In spiral cleavage, the geometric arrangement is more like stacking cannon balls or oranges, in that the 4 top cells are centered over the boundaries between the 4 bottom cells.

Ooplasmic segregation (cytoplasmic segregation)
(when the cleaving oocyte moves special cytoplasmic materials to certain locations, so that they only get put in certain cells, & these cells are caused to differentiate into muscle, or something)

The two best-studied examples of ooplasmic segregation are
polar lobes in snails and yellow crescents in sea squirts.

Snails and other molluscs, (& some worms) form polar lobes.
Polar lobes are large bumps that form on the surface of one of the cleaving cells, in some species during the first cleavage division, in other species during both of the first TWO cleave divisions and in a few species polar lobes form during all three of the first three cleavages.

After cleavage, the polar lobe cytoplasm goes into just one cell. This cell later differentiates into certain parts of the mesoderm. If you knock off the polar lobe, then mesoderm doesn't develop right.

But nobody has yet managed to discover how polar lobes are caused to form, or how they produce their effect (except that a contractile ring of acto-myosin causes formation of polar lobes, indicating that the cleavage mechanism itself is being used to redistribute whatever cytoplasmic factors cause mesoderm.)

In sea squirts, soon after fertilization, cortical cytoplasm rearranges spontaneously with (mysterious!) yellow-colored material forming a crescent.

The cells that get this material all differentiate into muscle cells.

Lots of excellent researchers have tried very hard to discover what special materials are in the yellow crescent & in polar lobes expecting the special materials would be transcription factors.

Mosaic development in contrast to regulative development.
These are yet another related category of differences between different kinds of animals in their cleavage stages of development.

Mosaic development ~= Highly determinate cell lineages:

Nematodes, snails, sea squirts and flies have very mosaic, non-regulative development.

Each C. elegans individual has exactly the same number of cells, and each cell has a certain totally consistent cell lineage.

I don't know whether cell number can also be constant in the big nematodes like Ascaris; does anyone in the class know? I do know that Rotifers and members of several other sub-phyla have exactly identical cell lineages (with genetic variations).

In sea urchin development, if you physically separate each of the first 4 cells can develop into a whole pluteus, with all parts reduced to 1/4 size. (and a quarter as many cells as usual) This really works well, and John Allen of this department is doing his PhD using this method to compare the ecology of normal, half-sized and quarter-sized embryos.

Frog embryos can be separated as late as the 2 cell stage.
Conversely, two when one-celled stages are squeezed together, sometimes they can develop into one double-sized tadpole (which is chimeric, please notice).

Mammal embryos can be separated or recombined as late as the eight cell stage or later, and still regulate. Mammal early embryology is probably the most regulative (= least mosaic) of any group of animals.

A central set of unsolved problem of embryology are

How does regulation work?
What is the causal difference between regulative vs. mosaic dev.
(Is the difference just when cell fate gets decided, late or early)
(Or are fundamentally different methods used?)
(cell-cell communication versus localization of cytoplasm)

Which is more similar to the other, flies or humans?
Do humans develop by the same mechanisms as flies, or is it the reverse?

Because many important genetic mechanisms of development have recently been discovered using flies, it is natural to conclude that these same mechanisms occur in humans.
On the other hand, some of these mechanisms seem to require that the early embryo be syncytial (as occurs in arthropods but not any vertebrate), and others would seem to predict only mosaic development.

Notice that several different kinds of mechanism can control which embryonic cell differentiates into which cell type.

A) Special materials stored in certain parts of the oocyte, during oogenesis.

B) Wherever the sperm enters the oocyte causes that region to behave differently.

C) Inductive signals from one cell to another (often much later in development) control differentiation (switch cells to a different type)

D) External signals, including gravity and light.

Several specific examples have been discovered of each of these different categories of control mechanisms.

Notice that when method A or B are used, then that species' eggs will tend to have mosaic development.

Conversely, that regulative development seems to depend on using method C (signalling between cells)

This is probably an oversimplification. But it is even more over-simplified to say that mosaic vs. regulative development is just a matter of whether cell fate is decided early or late.
These problems really haven't been solved yet.

Different kinds of mechanisms, etc. specific examples

A) Special materials stored in certain parts of the oocyte, during oogenesis.

A specific example:
In Drosophila, the m-RNA for the bicoid gene is stored in what will develop into the anterior end of the maggot.
The bicoid protein then forms a gradient from anterior to posterior
(the bicoid protein is a transcription factor!)

In some experiments, embryos with double the normal number of bicoid genes developed with more tissue becoming head.

But last year some other experiments found that flies developed normally even when the bicoid protein was irregular.
This was NOT expected! It is now claimed that some other mechanism "filters" the positional information, so that cells only respond the that part of the information that is correct!

Remember how genes are named for what goes wrong in mutants?
The "bic" gene is named because mutants are bicaudal (2 tails, no head)
The bicoid gene is named because its mutants resemble bic.

Researchers hoped & expected to find special transcription factors localized in the yellow crescent and the polar lobes etc.

But maybe that's not how they really work?

B) Wherever the sperm enters the oocyte causes that region to behave differently.

Specific examples:

In frogs, the point of sperm entry causes the blastopore (later) to form on whichever side of the blastula is opposite to where the sperm entered. After the sperm enters, the cortical cytoplasm actively shifts toward the side where the sperm entered, and this shift creates the "grey crescent" on the opposite side. Later, after cleavage, then the blastopore forms at the location of the grey crescent

Tricky experimenters tried fertilizing right at the animal pole; but in that case, they still develop a grey crescent, but use a different mechanism!! And when the experimenters avoided this second mechanism, the embryos had a fall-back mechanism (which hasn't been discovered yet)!!

In nematodes, whichever end the sperm enters will become the rear of the animal. This was discovered by UNC Biology Prof Bob Goldstein & S Hird: Development 122: pp 1467-1474 (1996)!