Are fatigue effects on the bilateral deficit speed dependent?
The failure of the size of the bilateral deficit to be comparable at 30 and 150 degreesxs(-1) following fatigue is contrary to previous published reports that suggested reduced activation of high threshold motor unit is the primary mechanism underlying the bilateral deficit.
The current model of cytokinin signaling emphasizes the essential role of conserved aspartate residue phosphorylation of RRBs in promoting cytokinin responses. Our comparative analyses of developmental and physiological traits of ARR1 and ARR1D94E overexpressing plants revealed that the ARR1D94E protein is indeed a constitutive and wide-spectrum cytokinin response activator.