Anti-CD79A (aa 33-140) polyclonal antibody

Observed phenotypic variation in living organisms is shaped by genomes, environment, and their interactions. Flowering time under natural conditions can showcase the diverse outcome of the gene-environment interplay. However, identifying hidden patterns and specific factors underlying phenotypic plasticity under natural field conditions remains challenging. With a genetic population showing dynamic changes in flowering time, here we show that the integrated analyses of genomic responses to diverse environments is powerful to reveal the underlying genetic architecture. Specifically, the effect continuum of individual genes (Ma(l), Ma(6), FT, and ELF3) was found to vary in size and in direction along an environmental gradient that was quantified by photothermal time, a combination of two environmental factors (photoperiod and temperature). Gene-gene interaction was also contributing to the observed phenotypic plasticity. With the identified environmental index to quantitatively connect environments, a systematic genome-wide performance prediction framework was established through either genotype-specific reaction-norm parameters or genome-wide marker-effect continua. These parallel genome-wide approaches were demonstrated for in-season and on-target performance prediction by simultaneously exploiting genomics, environment profiling, and performance information. Improved understanding of mechanisms for phenotypic plasticity enables a concerted exploration that turns challenge into opportunity.

We report that the protein kinase C iota (PKC iota) oncogene controls expression of NOTCH3, a key driver of stemness, in KRAS-mediated lung adenocarcinoma (LADC). PKC iota activates NOTCH3 expression by phosphorylating the ELF3 transcription factor and driving ELF3 occupancy on the NOTCH3 promoter. PKC iota-ELF3-NOTCH3 signaling controls the tumor-initiating cell phenotype by regulating asymmetric cell division, a process necessary for tumor initiation and maintenance. Primary LADC tumors exhibit PKC iota-ELF3-NOTCH3 signaling, and combined pharmacologic blockade of PKC iota and NOTCH synergistically inhibits tumorigenic behavior in vitro and LADC growth in vivo demonstrating the therapeutic potential of PKC iota-ELF3-NOTCH3 signal inhibition to more effectively treat KRAS LADC.