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Vena, R.

Publications and source records attributed to Vena, R..

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SCL28 promotes cell expansion and endoreplication in Arabidopsis by activating SIAMESE-RELATED cyclin-dependent kinase inhibitors.

The processes that contribute to plant organ morphogenesis are spatial-temporally organized. Within the meristem the mitotic cell cycle produces new cells that subsequently engage in specific cell expansion and differentiation programs once they exit the division competent zone. The latter is frequently accompanied by endoreplication, being an alternative cell cycle that replicates the DNA without nuclear division, causing a stepwise increase in somatic ploidy. We have previously shown that the Arabidopsis SCL28 transcription factor promotes progression through G2/M and modulates division plane orientation. Here, we demonstrate that SCL28 co-express and regulates genes specific to cell elongation and differentiation, including genes related to cell wall and cytoskeleton assembly. Consistently, this correlates with defects in post-mitotic cell expansion in a scl28 mutant. Strikingly, SCL28 controls expression of 6 members of the SIAMESE/SIAMESE-RELATED (SIM/SMR) family, encoding cyclin-dependent kinase inhibitors with a role in promoting mitotic cell cycle exit and endoreplication onset, both in response to developmental and environmental cues. Consistent with this role, scl28 mutants displayed reduced endoreplication, both in roots and leaves. Altogether, these results suggest that SCL28 controls cell expansion and differentiation by promoting endoreplication onset and by modulating aspects of the biogenesis, assembly and remodeling of the cytoskeleton and cell wall.

plant biology

AKAP350 REGULATES CYTOSKELETON REMODELLING AND LFA-1 ORGANIZATION DURING NK CYTOLYTIC RESPONSE

The elimination of transformed and viral infected cells by natural killer (NK) cells requires the formation of a specialized junction between NK and target cells, generally denominated immunological synapse (IS). After initial recognition, the IS enables the directed secretion of lytic granules content into the susceptible target cell. The lymphocyte function-associated antigen (LFA)-1 regulates NK effector function by enabling NK-IS assembly and maturation. The pathways underlying LFA-1 accumulation at the IS in NK cells have not been elucidated so far. A kinase anchoring protein 350 (AKAP350) is a centrosome/Golgi associated protein with a central role in the regulation of Golgi organization and microtubule dynamics. In T cells, AKAP350 participates in LFA-1 activation by mechanisms that remain elusive. We first investigated AKAP350 participation in NK cytolytic activity. Our results showed that the decrease in AKAP350 levels by expression of specific shRNAs (AKAP350KD) inhibited NK-YTS cytolytic activity, without affecting NK:target cell conjugate formation. The impairment of NK effector function in AKAP350KD cells correlated with decreased LFA-1 clustering and defective IS maturation. AKAP350KD cells that were exclusively activated via LFA-1 showed impaired LFA-1 organization and deficient lytic granule translocation as well. In NK AKAP350KD cells, activation signaling through Vav1 was preserved up to 10 min of interaction with target cells, but significantly decreased afterwards. Experiments in YTS and in ex vivo NK cells revealed the existence of an intracellular pool of LFA-1 vesicles, which partially associated with the Golgi apparatus. Upon NK cell activation, this LFA-1 pool redistributed to the IS in a Golgi-AKAP350-dependent manner. Disruption of Golgi integrity or alteration of microtubule dynamics impaired LFA-1 localization at the IS. Therefore, this study reveals the existence of a Golgi/AKAP350 dependent trafficking pathway for LFA-1, which is relevant for LFA-1 organization at NK-lytic IS and, concomitantly, for NK cytolytic function.

cell biology