Commentary on “Mandible exosomal ssc-mir-133b regulates tooth development in miniature swine via endogenous apoptosis”

This report,"Mandible exosomal ssc-mir-133b regulates tooth development in miniature swine via endogenous apoptosis" by Li et al. is an important step forward in describing the factors that control tooth development in a large animal model. That many of the regulatory miRNA pathways have been elucidated in murine species have always begged the question as to how relevant they

Magnaporthe Rab5 homologs show distinct functions in nerve growth factor(NGF)-mediated neurite outgrowth and cell differentiation

Nerve growth factor（NGF） binds to TrkA and forms a NGF/TrkA complex at the cell surface,which is then internalized into signaling endosomes and promotes neuronal survival and neurite outgrowth.The small GTPase Rab5 is reported to localize on the plasma membrane and early endosomes,regulating endosome fusion.It was reported that endogenous Rab5 function may need to be suppressed during NGF-induced neurite outgrowth and cell differentiation.Two Rab5 homologs（MoRab5A：MGG_06241 and MoRab5B：MGG_01185） were characterized from the rice blast fungus Magnaporthe oryzae,and MoRab5 B was identified as the Rab5 ortholog promoting early endosomal fusion,while MoRab5 A specialized to perform a non-redundant function in endosomal sorting.In this study,we examined whether MoRab5 A and MoRab5 B play different roles in NGF-induced neurite outgrowth and cell differentiation in PC12 cells（a rat pheochromocytoma cell line）.Our data showed that MoRab5 B is a negative regulator of NGF signaling and neurite outgrowth in PC12 cells,similar to human Rab5（hRab5）.MoRab5B：WT inhibits NGF signaling-dependent neurite outgrowth while the dominant-negative MoRab5 B mutant（MoRab5B：DN） enhances NGF signaling and neurite outgrowth.In contrast,MoRab5A：WT and MoRab5A：DN both significantly promote NGF-induced neurite outgrowth,indicating that MoRab5 B is more similar to hRab5 than MoRab5 A in the regulation of NGF signal transduction.

An auxin‐responsive endogenous peptide regulates root development in Arabidopsis

Auxin plays critical roles in root formation and development. The components involved in this process, however, are not well understood. Here, we newly identified a peptide encoding gene, auxin-responsive endogenous polypeptide 1 （AREP1）, which is induced by auxin, and mediates root development in Arabidopsis. Expression of AREP1 was specific to the cotyledon and to root and shoot meristem tissues. Amounts of AREP1 transcripts and AREP1-green fluorescent protein fusion proteins were elevated in response to indoleacetic acid treatment. Suppression of AREP1 through RNAi silencing resulted in reduction of primary root length, increase of lateral root number, and expansion of adventitious roots, compared to the observations in wild-type plants in the presence of auxin. By contrast, transgenic plants overexpressing AREP1 showed enhanced growth of the primary root under auxin treatment. Additionally, rootmorphology, including lateral root number and adventitious roots, differed greatly between transgenic and wildtype plants. Further analysis indicated that the expression of auxin-responsive genes, such as IAA3, IAA7, IAA17, GH3.2, GH3.3, and SAUR-AC1, was significantly higher in AREP1 RNAi plants, and was slightly lower in AREP1 overexpressing plants than in wildtype plants. These results suggest that the novel endogenous peptide AREP1 plays an important role in the process of auxinmediated root development.

FERM domain phosphorylation and endogenous 3＇UTR are not essential for regulating the function and subcellular localization of polarity protein Crumbs

In the past two decades, extensive studies have focused on a group of so-called polarity proteins that play conserved and essential functions in establishing and maintaining cell polarity in epithelial cells. Among them, Crumbs （Crb） is the only trans- membrane polarity protein characterized to date （Tepass et al.,

Arabidopsis SUMO protease ASP1 positively regulates flowering time partially through regulating FLC stability

The initiation of flowering is tightly regulated by the endogenous and environment signals, which is crucial for the reproductive success of flowering plants. It is well known that autonomous and vernalization pathways repress transcription of FLOWERING LOCUS C（FLC）, a focal floral repressor, but how its protein stability is regulated remains largely unknown. Here, we found that mutations in a novel Arabidopsis SUMO protease 1（ASP1） resulted in a strong late-flowering phenotype under long-days, but to a lesser extent under short-days. ASP1 localizes in the nucleus and exhibited a SUMO protease activity in vitro and in vivo. The conserved Cys-577 in ASP1 is critical for its enzymatic activity, as well as its physiological function in the regulation of flowering time. Genetic and gene expression analyses demonstrated that ASP1 promotes transcription of positive regulators of flowering, such as FT,SOC1 and FD, and may function in both CO-dependent photoperiod pathway and FLC-dependent pathways.Although the transcription level of FLC was not affected in the loss-of-function asp1 mutant, the protein stability of FLC was increased in the asp1 mutant. Taken together, this study identified a novel bona fide SUMO protease, ASP1,which positively regulates transition to flowering at least partly by repressing FLC protein stability.