The blooms on the Haemanthus pauculifolius are fraying, and they will be the last Haemanthus to bloom until H. montanus blooms in June. At the same time, Scadoxus puniceus are starting to show signs of life, and one of them has a scape half way up. They usually bloom somewhere between late January and early March in the cool greenhouse (low temperatures dip into the high 30s F).

In the warm greenhouse (pretty constant at about 55 ° F) only Nerine undulata is in bloom. We won't see any new Nerine flowers now until sometime in July, once the undulata fade. I've had some small N. humilis growing for several years, but they do not seem to get much larger, they do not flower, and I suspect they have a viral or a fungal disease. I will probably have to get rid of them.

My Nerine sarniensis hybrids are looking good. Taking a tip from Nick de Rothschild, I tried feeding them, using soluble fertilizer with 0% nitrogen. They have perked up tremendously! I formulated my own fertilizer, using finely crystalline reagent grades of Dibasic Potassium Phosphate (i.e., K₂HPO₄ ), Monobasic Potassium Phosphate (i.e., KH₂PO₄ ), and Potassium Sulfate (i.e., K₂SO₄ ), very thoroughly dry mixed. I used equal parts by weight of each of the three chemicals, giving a moderate level of phosphate (P) and a high dose of potassium (K). I dissolve about ½ teaspoonful of the mixture in 1200 mL (about 5 cups) of water. We have to avoid using more than tiny traces of nitrogen on the broadleaf Nerine species and hybrids, because feeding them nitrogen seems to release latent virus infections that they all carry. You can ruin a collection of broadleaf Nerine (i.e., hybrids of Nerine bowdenii, sarniensis, and several others) by dumping a little bit of nitrogen on them.

I'm using mostly the names of the genes as they were described for the dwarf cress, Arabidopsis thaliana, which is the "lab rat" or "fruit fly" for plant biologists. Arabidopsis thaliana is a small species, easy to propagate in the lab, with a few large chromosomes, and one from which it has been possible to isolate a large number of mutants.

Almost 20 years ago, it was found that there are a set of specific genes that lead a new shoot to form a flower. Because there were initially three general types found, they were referred to as the A, B, and C classes. If you inactivated certain of the genes, you did not get any petals in the flower. This was therefor called APETALA. When it was found that there were two genes that caused loss of petals when mutated, they ended up with APETALA1 (AP1) and APETALA3 (AP3). It turns out that you need two classes of genes to make petals: A and also B. APETALA1 is the A gene and APETALA3 is one of the B genes. APETALA probably comes from "a-" meaning without and "petal." A second B gene was found, and given the name PISTILLATA (PI). I haven't tracked down where that name came from. It turns out that there have to be functioning copies of both the B genes in order to have full, normal flower development. APETALA3 and PISTILLATA form what is called a "heterodimer," e.g., a structure made up of two protein molecules that are not identical.

The C gene is necessary for formation of the sexual parts of the flower. When it is mutated, there are no stamens and no pistil, so it was named AGAMOUS (AG). If one of the B genes is mutated, you get the pistil but no stamens. The formation of stamens therefor requires functional B genes and the C gene. The C gene alone is needed for formation of the pistil.

When the A, B, and C genes are expressed ectopically (in non-flower parts of the plant), there are no flower parts formed. This indicated that more genes are needed to get sepals, petals, stamens, or pistils than just the ABC set.

The Scheme for Floral Gene Interactions

Those additional genes are now referred to as the SEPALLATA (SEP) genes, and are often called the E class of genes. There are 4 of these genes, SEP1, SEP2, SEP3, and SEP4. These function somewhat redundantly, but in the absence of all 4 of the SEP genes, there are no flower parts produced. Which SEP genes are expressed depends on when and where one looks. The discovery that a fourth class of genes is required has led to recent papers calling this the "ABCE" model.

The "quartet model" for how these gene product work is based on studies of protein-protein interactions. The quartet AP1-AP1-SEP-SEP leads to formation of sepals. The quartet AP1-AP3-PI-SEP leads to petals; AP3-PI-AG-SEP induces stamens; and AG-AG-SEP-SEP forms carpels (ovary and pistil). Protein chemists would refer to these quartets as tetramers, since the four separate protein molecules involved are physically associated with each other.

All of these genes are members of the MADS-box family (except for AP2). The MADS structure is named for the four very different species in which such genes were found: Mouse, Arabidopsis, Drosophila (fruit fly), and Saccharomyces (yeast). MADS genes have also been found in mammals, including humans. This is clearly a very old motif in the history of life.

In the early 1980s, I read a fascinating little book by Vern Grant, called "Plant Speciation." It laid out, in what I thought was a fairly straight forward way, where new plant species might come from. Among the cases in point were the rain lilies. Grant used them as examples of new species arising from polyploidy and from parthenogenic mechanisms.