The phrase "autonomous contributions" is correct and usable in written English.
It can be used to refer to contributions made independently or without external control, often in contexts related to teamwork, research, or individual efforts.
Example: "The project was successful due to the autonomous contributions of each team member, allowing for diverse ideas and solutions."
Alternatives: "independent contributions" or "self-directed contributions".
Thus, in addition to its role as NOTCH ligand in maintaining the self-replicating state of the adjacent NP cells, our results indicate that Delta-1 may have a cell autonomous contribution to the switch to neurogenic NP cells as indicated by the cell autonomous induction of Tis21.
This suggests a non-cell autonomous contribution to the vascular phenotype in Foxc1 mutant mice.
There is accumulating experimental evidence of non-cell-autonomous contributions of cells other than motor neurons to ALS pathology.
At this point, non-autonomous contributions to the oligodendrocyte-axon system could not be discounted because MCT1 is also expressed in other cell types (albeit at low levels).
Notably, this phenotype depends on the expression of these signaling molecules in hematopoietic progenitor cells that give rise to circulating endothelial progenitor cells, thus demonstrating a cell-autonomous contribution of hematopoietic cells to vascular development [11], [12].
Importantly, the cell-autonomous contribution of VDR to osteoblastic differentiation has been demonstrated by several additional lines of evidence.
Although our model is not osteoblast specific, we have ruled out the cell-autonomous contribution of chondrocytes or osteoclasts in these processes in our mice.
Genetic ablation of retinal microglia, pharmacological inhibition of microglial phagocytosis, as well as inhibition of IL-1β signaling, all slow down rod degeneration, demonstrating the non-cell-autonomous contribution that microglia make to photoreceptor degeneration in RP.
However, our model differs from existing continuum models in several ways: it is directly based on measurable cellular contributions to tissue shear, it includes a new time scale corresponding to a delay for the generation of T1 transitions, and it introduces a cell-autonomous contribution to T1 transitions.
The non-cell-autonomous contribution of microglia is evidenced by the morphological and functional amelioration of photoreceptor degeneration upon the genetic ablation of retinal microglia and the molecular inhibition of microglial phagocytosis, indicating that microglial phagocytosis of living rods contributes to inherited photoreceptor degeneration.
