Fsd2, or Fibronectin Type III and SPRY Domain Containing 2, is associated with multiple biological functions. In plants like Arabidopsis thaliana, it is a chloroplast-localized iron superoxide dismutase, functioning in detoxifying superoxide, protecting chloroplast nucleoids from oxidative stress, and being essential for early chloroplast development [1,2,6,7]. In pigs, it's considered a candidate gene for pork quality, with its haplotypes related to intramuscular fat content, moisture percentage, and meat color [4]. In mammals, it's part of the myospryn complex in cardiac and skeletal muscle, interacting with proteins like Speg and Cmya5, and playing a role in stabilizing excitation-contraction coupling protein complexes [3,5,8].

In Arabidopsis, loss-of-function mutants of Fsd2 exhibit increased superoxide production, reduced chlorophyll levels, lower photosynthetic efficiency, and impaired growth [1]. In pap9/fsd2 mutants, under heat stress, there are declines in chlorophyll content and photosynthesis level, and abnormal regulation of photosynthesis-related genes [2]. In mice, Speg deficiency leads to a decrease in Fsd2 protein levels, accompanied by defective triad formation, abnormal excitation-contraction coupling, and calcium mishandling in skeletal muscles [5].

In summary, Fsd2 plays crucial roles in plant photosynthesis-related stress responses and in maintaining the stability of muscle-related protein complexes in animals. The study of Fsd2 through gene-knockout models in plants and mice has provided insights into its functions in these biological processes, which may have implications for understanding plant stress-tolerance mechanisms and muscle-related diseases.