Consider an age-dependent, single-species branching process defined by a progeny number distribution, and a lifetime distribution associated with each independent particle. In this paper, we focus on the associated inverse problem where one wishes to formally solve for the progeny number distribution or the lifetime distribution that defines the Bellman-Harris branching process. We derive results for the existence and uniqueness (the identifiability) of these two distributions given one of two types of information: the extinction time probability of the entire process (extinction time distribution), or the distribution of the total number of particles at one fixed time. We demonstrate that perfect knowledge of the distribution of extinction times allows us to formally determine either the progeny number distribution or the lifetime distribution. Furthermore, we show that these constructions are unique. We then consider “data” consisting of a perfectly known total number distribution given at one specific time. For a process with known progeny number distribution and exponentially distributed lifetimes, we show that the rate parameter is identifiable. For general lifetime distributions, we also show that the progeny distribution is globally unique. Our results are presented through four theorems, each describing the constructions in the four distinct cases.

We study generalized Hopf–Cole transformations motivated by the Schrödinger bridge problem, which can be seen as a boundary value Hamiltonian system on the Wasserstein space. We prove that generalized Hopf–Cole transformations are symplectic submersions in the Wasserstein symplectic geometry. Many examples, including a Hopf–Cole transformation for the shallow water equations, are given. Based on this transformation, energy splitting inequalities are provided.

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The stochasticity of gene expression is manifested in the fluctuations of mRNA and protein copy numbers within a cell lineage over time. While data of this type can be obtained for many generations, most mathematical models are unsuitable to interpret such data since they assume non-growing cells. Here we develop a theoretical approach that quantitatively links the frequency content of lineage data to subcellular dynamics. We elucidate how the position, height, and width of the peaks in the power spectrum provide a distinctive fingerprint that encodes a wealth of information about mechanisms controlling transcription, translation, replication, degradation, bursting, promoter switching, cell cycle duration, cell division, gene dosage compensation, and cell size homeostasis. Predictions are confirmed by analysis of single-cell Escherichia coli data obtained using fluorescence microscopy. Furthermore, by matching the experimental and theoretical power spectra, we infer the temperature-dependent gene expression parameters, without the need of measurements relating fluorescence intensities to molecule numbers.

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