Linnaeus' flower clock was a garden plan hypothesized by Carolus Linnaeus that would take advantage of several plants that open or close their flowers at particular times of the day to accurately indicate the time.

My research in this area is very much concerned with understanding the design principles of circadian clocks. What are their roles and how is this reflected in their structure? I would add that since the clock is a dynamical system with a very complex molecular structure and since the role of the clock is clearly multifacited, this cannot be answered without the use of mathematics. My collaborators are listed here.

The circadian clock adapts organisms to the environmental day-night cycle both behaviorally and physiologically. In animals, not only are complex behaviors such as sleep and mood governed by this oscillator, but also different body functions such as digestion, circulation, and respiration. The basic mechanism of this clock is cell-autonomous in all studied species possessing a circadian clock i.e. each cell contains a network of genes and proteins that can generate an oscillator with a period of approximately 24 hours. These oscillators can, in turn be entrained, to the relevant 24-hour environmental day-night cycle.

In mammals, individual clocks in most cells are synchronized by a brain “master clock” in the suprachiasmatic nucleus of the hypothalamus. This orchestrates all rhythmic physiology and signals from this master clock entrain the clocks in peripheral cells. This global system is often referred to a the Circadian Timing System. It should be thought of as the body'd metronome as explained in this INSERM article.

In humans, disruption of the circadian rhythm is associated with sleep disorders and many other diseases including cancer, obesity and diabetes. On a cellular level, circadian physiology extends even to processes such as proliferation, apoptosis, and DNA damage repair, which are thought to play important roles in cancer initiation and control.

In plants there is no such "master clock" but the cellular circadian clock is entrained by the cycles of light and dark, and temperature. The light input pathway to the clock is complex and only just becoming understood.
Besides vertebrates and plants most many other species have such circadian clocks including flies, fungi, and bacteria.

In individual cells, the circadian clock mechanism consists of oscillating feedback loops of transcription of “core” oscillator genes and posttranslational modifications of their protein products that regulate protein stability, activity, and/or localization.

The majority of clock components are transcriptional activators or repressors that modulate protein stability and nuclear translocation, and create two interlocking feedback loops. In the first, CLOCK and BMAL1, heterodimerize in the cytoplasm to form a complex that, following translocation to the nucleus, initiates transcription of target genes such as the core clock genes Period genes (PER1, PER2, and PER3) and two Cryptochrome genes (CRY1 and CRY2).

Negative feedback is achieved by PER:CRY heterodimers that translocate back to the nucleus to repress their own transcription by inhibiting the activity of the CLOCK:BMAL1 complexes. Another regulatory loop is induced when CLOCK:BMAL1 heterodimers activate the transcription of Rev-ErbA and Rora, two retinoic acid-related orphan nuclear receptors. REV-ERBa and RORa subsequently compete to bind retinoic acid-related orphan receptor response elements (ROREs) present in Bmal1 promoter. Through the subsequent binding of ROREs, members of ROR and REV-ERB are able to regulate Bmal1. While RORs activate transcription of Bmal1, REV-ERBs repress the same transcription process. Hence, the circadian oscillation of Bmal1 is both positively and negatively regulated by RORs and REV-ERBs.

The two morning-specific MYB transcription factors, LATE ELONGATED HYPOCOTYL (LHY) and CIRCADIAN CLOCK ASSOCIATED-1 (CCA1) act to repress expression of a pseudo response regulator (PRR1, also known as TIMING OF CAB-1, or TOC1) during the day, by binding to an Evening Element (EE) motif in the promoter of its gene.

As LHY/CCA1 protein levels decline towards the evening, TOC1 accumulates and acts to repress transcription from their respective promoters. Expression of LHY and CCA1 mRNAs resumes towards dawn, when this repression is lifted, through down-regulation of TOC1 transcription by an Evening Complex (EC) composed of three proteins, LUX and EARLY FLOWERING (ELF) 3 and 4. In addition to TOC1, three other PRR proteins (PRR9, 7 and 5) are expressed sequentially throughout the day (4). Each of these proteins binds to the LHY and CCA1 promoters to repress their activity, and their combined effect over the course of the circadian cycle ensures that this inhibition is maintained from the late morning until the following dawn (5).

A key problem that I am trying to address is why the regulatory networks of these clocks almost universally have a highly complicated structure, with multiple interlocking positive and negative feedback loops when a simple negative feedback loop can reliably produce robust oscillations. My basic hypothesis is that it is to enable the flexibility to respond in multiple ways to multiple evolutionary demands some of which will conflict such as in the following examples