An alternative cell-fate hypothesis (Russo et al. 2008; Sivaraman and Medina 2002) proposes that the hormones of pregnancy induce a molecular switch in stem cells that produces cells with persistent changes in regulatory pathways that control proliferation and response to DNA damage.
The steadily increasing expression of mature photoreceptor markers supports a fate change hypothesis for the effect of taurine/RA on RSC differentiation (see Discussion).
The conservation of the identical temporal sequence of Nrl/rhodopsin expression regardless of the presence of a two-week expansion of retinal precursors from RSCs in 1%FBS+F/H ([1%FBS+F/H]/[T+RA+F/H] sequence, Fig. 2I,J) supports a fate change hypothesis, but does not in itself rule out a selective photoreceptor survival effect.
To resolve the role of autophagy in cancer cell fate, several hypotheses have been put forward.
The identification of fate- and direction of rotation-specific genes would support the hypothesis that fate specification and direction of rotation can be genetically uncoupled.
Lineage commitment in the mammalian embryo is most often depicted as a series of binary choices between alternate cell states, and increasing evidence supports the hypothesis that fate decisions in embryonic stem (ES) cell cultures reflect these developmental processes [1].
It further corroborates the hypothesis that the fate of the species may be considerably affected by its core attractiveness to humans.
This interpretation of the origin of these subclasses of mutant ommatidia (specifically the A/P and AP/DV defects) supports the hypothesis that cell fate and direction of rotation can be uncoupled, as follows (and as described in [3]).
These findings support the hypothesis regarding evolutional fate of duplicate genes, i.e. there is functional diversity and redundancy in OsRFP genes.
The present study shows some evidence of stemness and cell plasticity in tamoxifen-resistant cells and poses a new hypothesis linking cell fate plasticity, epigenetic programming, and possible induced pluripotency processes with tamoxifen resistance.
This somatic cell-dominated sex differentiation model expands the previous hypothesis that ovarian fate is passively determined by a threshold number of developing oocytes; that is, a number of oocytes exceeding the threshold activate the female pathway, whereas a number of oocytes under the threshold induce the male pathway.
