MECHANISTIC MODEL OF TEMPERATURE INFLUENCE ON FLOWERING THROUGH WHOLE-PLANT ACCUMULATION OF FT
In this paper, we assessed temperature influence on flowering by incorporating temperature-responsive flowering mechanisms across developmental age into an existing model. Temperature influences both the leaf production rate and expression of FLOWERING LOCUS T (FT), a photoperiodic flowering regulator, in leaves. The Arabidopsis Framework Model incorporated temperature influence on leaf growth but ignored the consequences of leaf growth on and direct temperature influence of FT expression. We measured FT production in differently aged leaves and modified the model, adding the mechanistic temperature influence on FT transcription, and linking FT to leaf growth. Our simulations suggest that in long days, the developmental timing (leaf number) at which the reproductive transition occurs is influenced by day length and temperature through FT, while temperature influences the rate of leaf production and the time (in days) the transition occurs. Further, we demonstrated that FT is mainly produced in the first 10 leaves in the Columbia ecotype, and that FT accumulation alone cannot explain flowering in conditions in which flowering is delayed. Our simulations supported our hypotheses that: 1) temperature regulation of FT, accumulated with leaf growth, is a component of thermal time, and 2) incorporating mechanistic temperature regulation of FT can improve model predictions in fluctuating temperatures.
Molecular basis of EMRE-dependence of the human mitochondrial calcium uniporter
The mitochondrial uniporter is calcium-activated calcium channel complex critical for cellular signaling and bioenergetics. MCU, the pore-forming subunit of the uniporter, contains two transmembrane domains and is found in all major eukaryotic taxa. In amoeba and fungi, MCU homologs are sufficient to form a functional calcium channel, whereas human MCU exhibits a strict requirement for the metazoan-specific, single-pass transmembrane protein EMRE for conductance. Here, we exploit this evolutionary divergence to decipher the molecular basis of EMRE dependence of human MCU. By systematically generating chimeric proteins that consist of EMRE-independent D. discoideum MCU (DdMCU) and H. sapiens MCU (HsMCU), we converged on a stretch of 10 amino acids in DdMCU that can be transplanted to HsMCU to render it EMRE-dependent. We call this region in human MCU the EMRE-dependence domain (EDD). Crosslinking experiments show that HsEMRE directly interacts with MCU at both of its transmembrane domains as well as the EDD. Based on previously published structures of fungal MCU homologs, the EDD segment is located distal to the selectivity filter of the calcium pore and appears flexible. We propose that EMRE stabilizes EDD of MCU, permitting both channel opening and calcium conductance