Scanning Electron Microscopy of the Rainbow Trout (Salmo gairdneri Richardson) Spermatozoon

The scanning electron microscope was used to determine the morphology of the rainbow trout (Salmo gairdneri Richardson) spermatozoon. The spermatozoon is approximately 32 μm long and consists of a head, mitochondrial collar, and flagellum. The head is elongated and somewhat flattened. It has an antero posterior length of 3.1 μm and a maximum diameter of 1.6 to 2.2 μm. Mean antero-posterior length of the mitochondrial collar is 0.8 μm The collar encircles the flagellum but is separated from it. The flagellum ranges in length from 26 to31 μm and is divided into a principal piece and end piece. Cytoplasmic vesicles commonly are found in the anterior region of the flagellu

Quantification of protein abundance and interaction defines a mechanism for operation of the circadian clock

The mammalian circadian clock exerts control of daily gene expression through cycles of DNA binding. Here, we develop a quantitative model of how a finite pool of BMAL1 protein can regulate thousands of target sites over daily time scales. We used quantitative imaging to track dynamic changes in endogenous labelled proteins across peripheral tissues and the SCN. We determine the contribution of multiple rhythmic processes coordinating BMAL1 DNA binding, including cycling molecular abundance, binding affinities, and repression. We find nuclear BMAL1 concentration determines corresponding CLOCK through heterodimerisation and define a DNA residence time of this complex. Repression of CLOCK:BMAL1 is achieved through rhythmic changes to BMAL1:CRY1 association and high-affinity interactions between PER2:CRY1 which mediates CLOCK:BMAL1 displacement from DNA. Finally, stochastic modelling reveals a dual role for PER:CRY complexes in which increasing concentrations of PER2:CRY1 promotes removal of BMAL1:CLOCK from genes consequently enhancing ability to move to new target sites

Quantification of protein abundance and interaction defines a mechanism for operation of the circadian clock.

The mammalian circadian clock exerts control of daily gene expression through cycles of DNA binding. Here, we develop a quantitative model of how a finite pool of BMAL1 protein can regulate thousands of target sites over daily time scales. We used quantitative imaging to track dynamic changes in endogenous labelled proteins across peripheral tissues and the SCN. We determine the contribution of multiple rhythmic processes coordinating BMAL1 DNA binding, including cycling molecular abundance, binding affinities, and repression. We find nuclear BMAL1 concentration determines corresponding CLOCK through heterodimerisation and define a DNA residence time of this complex. Repression of CLOCK:BMAL1 is achieved through rhythmic changes to BMAL1:CRY1 association and high-affinity interactions between PER2:CRY1 which mediates CLOCK:BMAL1 displacement from DNA. Finally, stochastic modelling reveals a dual role for PER:CRY complexes in which increasing concentrations of PER2:CRY1 promotes removal of BMAL1:CLOCK from genes consequently enhancing ability to move to new target sites