Flowering is initiated in grasses when the developmental program at the shoot apical meristem switches from producing vegetative to reproductive structures. The switch occurs via endogenous controls and in response to cues from the environment. Day-length is a major factor controlling flowering time and it is commonly believed to generate a signal in the green leaves which is transferred to the shoot apical meristem. Whether the signal is the flowering hormonal complex ‘florigen’, an electrical signal, or a multi-factorial process involving phytohormones and sugars remains inadequately backed by research. Many genes are said to control the onset of flowering in plants but the physiological mechanisms that switch those genes on-and-off remain hidden. Recent evidence shows that small signaling molecules may be implicated in but again not necessarily causal to the flowering process. In the monocotyledon Sorghum bicolor the elongation rates of leaf primordia and of unexposed leaves (those wholly within the whorl) slowed during the vegetative developmental phase during a defined period prior to the initiation of panicle structures. The response was the same in treatments where the timing of panicle initiation was varied by season, agronomy, photoperiod, cultivar or defoliation. Moreover, in all treatments, panicle initiation was coincident to the attainment of both a common architecture of the shoot apex and comparable slowing of the elongation rates of leaf primordia and unexposed leaves. During vegetative development the total length of unexposed leaves was strongly dependent on the area of green leaf. We hypothesize that growth-related processes that slowed the elongation rate of leaf primordia and unexposed leaves might also have triggered panicle initiation. In a hereditary sense, this effect would ensure that the plant had sufficient leaf area and vegetative biomass to grow seed, in the same trend that those similar ancestors had adequate plant architecture and thus reproduced and survived.