As for future possible developments, we make the hypothesis that both the speed-curvature co-variation at the level of motor primitives, and the adoption of diverse sensory-motor strategies (e.g. different sequences of motor units such as combined deceleration-steering versus braking-steering) aim at robust control, i.e., the minimum variance principle introduced by Harris and Wolpert.
In order to highlight interesting transcription factors that may be active in the embryo development, we made a correspondence analysis between probe set expression and the motifs at the binding sites of the promoter of the genes they interrogate [20].
To further assess a potential role of Gfi1 in early lymphoid development, we made use of a transgenic Gfi1GFP/Gfi1 reporter mouse that allows monitoring of the transcriptional activity of the Gfi1 locus.
In order to study MADS domain proteins in living tissues with CLSM during floral development, we made C-terminal GFP tagged versions of SEP3, AG, FUL, and AP1.
To identify the drivers underlying the gains and losses selected for during breast cancer development, we made use of the synteny between human and mouse genomes [ 30].
To distinguish between the divergent functions of β-catenin during peripheral nervous system development, we made use of a mutant allele of β-catenin that can mediate adhesion but not Wnt-induced TCF transcriptional activation.
To investigate whether T3 actions in the epithelium and non-epithelium have specific roles in adult intestinal stem cell development, we made use of a transgenic Xenopus laevis line that expresses a dominant positive TR under the control of a heat shock-inducible promoter for organ culture studies.
The developments we have made can drastically rebalance the time distribution of scientists examining the structures of complex materials, away from monotonous, repetitive, operator-biased modalities of image processing towards interpretation of vast, rich quantitative results.
To characterize the activity of p66 and assess its importance in mouse development, we have made loss of function mutants in the mouse p66α gene (mp66α, official name Gatad2a, MGI 2384585).
In an effort to give access to cardiac fated populations at the earliest stages of development, we have made use of a transgenic mESC line (Nkx2-5-GFP) contanning an established cardiac specific enhancer element of the Nkx2-5 transcription factor [15] driving expression of the green fluorescent protein (Methods).
