The vegetative apex was a low dome consisting of two layers of tunica surmounting a very small corpus. Foliar primordia originated as periclines in the flanks of T2. The transition apex became first a steep cone and then a hemisphere. All floral primordia—the two bracts, the two sepals, the several whorls of petals, the several whorls of stamens, and the carpels—originated in the manner of leaves, as periclines in T2 on the flanks of the apex. All appendages, including carpels, were therefore lateral. In the early transition, the apex had a brief stage in which there were three tunica layers, but the inner one was lost with the onset of the sepals. The bracts and the first sepal continued the normal positions of primordia for the vegetative phyllotaxy of 3/8, but with the second sepal, this phyllotaxy was lost, and petals, stamens, and carpels were produced in whorls. While leaves, bracts, sepals, and petals were produced in acropetal sequence, stamens were produced in basipetal sequence, and carpels appeared simultaneously. After carpels were formed, the rest of the floral apex underwent a brief period of expansion growth, achieving a diameter comparable to that of a shoot apex, but its substance was eventually incorporated into the carpel margins, which later produced the ovules. This agrees with the determinate nature of the floral apex. During the development of the first series of floral organs, the floral apex underwent continued increase in area, finally achieving a diameter several times that of the vegetative shoot apex. Its size and form were such that they were compared to those of some inflorescence apices. After development of the first series of floral organs, the subjacent tissues to the floral meristem underwent divisions and elongation at right angles to the axis, causing at first a flattening of the meristem, and eventually a cup-shaped form, with the carpels attached in the bottom of a bowl. The mature flower was thus perigynous, but this development arose quite differently from the perigyny as it is known from ontogenetic studies in the Rosaceae.
Gammaherpesvirus infection modulates the temporal and spatial expression of SCGB1A1 (CCSP) and BPIFA1 (SPLUNC1) in the respiratory tract
