@article{MunozManganoPazGonzalezGarciaetal.2017,
  author    = {Mu{\~n}oz, Alfonso and Mangano, Silvina and Paz Gonzalez-Garcia, Mary and Contreras, Ramon and Sauer, Michael and De Rybel, Bert and Weijers, Dolf and Juan Sanchez-Serrano, Jose and Sanmartin, Maite and Rojo, Enrique},
  title     = {RIMA-Dependent Nuclear Accumulation of IYO Triggers Auxin-Irreversible Cell Differentiation in Arabidopsis},
  series = {The plant cell},
  volume    = {29},
  journal   = {The plant cell},
  number    = {3},
  publisher = {American Society of Plant Physiologists},
  address   = {Rockville},
  issn      = {1040-4651},
  doi       = {10.1105/tpc.16.00791},
  pages     = {575 -- 588},
  year      = {2017},
  abstract  = {The transcriptional regulator MINIYO (IYO) is essential and rate-limiting for initiating cell differentiation in Arabidopsis thaliana. Moreover, IYO moves from the cytosol into the nucleus in cells at the meristem periphery, possibly triggering their differentiation. However, the genetic mechanisms controlling IYO nuclear accumulation were unknown, and the evidence that increased nuclear IYO levels trigger differentiation remained correlative. Searching for IYO interactors, we identified RPAP2 IYO Mate (RIMA), a homolog of yeast and human proteins linked to nuclear import of selective cargo. Knockdown of RIMA causes delayed onset of cell differentiation, phenocopying the effects of IYO knockdown at the transcriptomic and developmental levels. Moreover, differentiation is completely blocked when IYO and RIMA activities are simultaneously reduced and is synergistically accelerated when IYO and RIMA are concurrently overexpressed, confirming their functional interaction. Indeed, RIMA knockdown reduces the nuclear levels of IYO and prevents its prodifferentiation activity, supporting the conclusion that RIMA-dependent nuclear IYO accumulation triggers cell differentiation in Arabidopsis. Importantly, by analyzing the effect of the IYO/RIMA pathway on xylem pole pericycle cells, we provide compelling evidence reinforcing the view that the capacity for de novo organogenesis and regeneration from mature plant tissues can reside in stem cell reservoirs.},
  language  = {en}
}
@article{RobertGrunewaldSaueretal.2015,
  author    = {Robert, Helene S. and Grunewald, Wim and Sauer, Michael and Cannoot, Bernard and Soriano, Mercedes and Swarup, Ranjan and Weijers, Dolf and Bennett, Malcolm and Boutilier, Kim and Friml, Jiri},
  title     = {Plant embryogenesis requires AUX/LAX-mediated auxin influx},
  series = {Development : Company of Biologists},
  volume    = {142},
  journal   = {Development : Company of Biologists},
  number    = {4},
  publisher = {Company of Biologists Limited},
  address   = {Cambridge},
  issn      = {0950-1991},
  doi       = {10.1242/dev.115832},
  pages     = {702 -- 711},
  year      = {2015},
  abstract  = {The plant hormone auxin and its directional transport are known to play a crucial role in defining the embryonic axis and subsequent development of the body plan. Although the role of PIN auxin efflux transporters has been clearly assigned during embryonic shoot and root specification, the role of the auxin influx carriers AUX1 and LIKE-AUX1 (LAX) proteins is not well established. Here, we used chemical and genetic tools on Brassica napus microspore-derived embryos and Arabidopsis thaliana zygotic embryos, and demonstrate that AUX1, LAX1 and LAX2 are required for both shoot and root pole formation, in concert with PIN efflux carriers. Furthermore, we uncovered a positive-feedback loop between MONOPTEROS-(ARF5)dependent auxin signalling and auxin transport. This MONOPTEROS dependent transcriptional regulation of auxin influx (AUX1, LAX1 and LAX2) and auxin efflux (PIN1 and PIN4) carriers by MONOPTEROS helps to maintain proper auxin transport to the root tip. These results indicate that auxin-dependent cell specification during embryo development requires balanced auxin transport involving both influx and efflux mechanisms, and that this transport is maintained by a positive transcriptional feedback on auxin signalling.},
  language  = {en}
}