Regulation Of Elongation Research Articles

Karrikin Signaling Acts Parallel to and Additively with Strigolactone Signaling to Regulate Rice Mesocotyl Elongation in Darkness.

Seedling emergence in monocots depends mainly on mesocotyl elongation, requiring coordination between developmental signals and environmental stimuli. Strigolactones (SLs) and karrikins are butenolide compounds that regulate various developmental processes; both are able to negatively regulate rice (Oryza sativa) mesocotyl elongation in the dark. Here, we report that a karrikin signaling complex, DWARF14-LIKE (D14L)-DWARF3 (D3)-O. sativa SUPPRESSOR OF MAX2 1 (OsSMAX1) mediates the regulation of rice mesocotyl elongation in the dark. We demonstrate that D14L recognizes the karrikin signal and recruits the SCFD3 ubiquitin ligase for the ubiquitination and degradation of OsSMAX1, mirroring the SL-induced and D14- and D3-dependent ubiquitination and degradation of D53. Overexpression of OsSMAX1 promoted mesocotyl elongation in the dark, whereas knockout of OsSMAX1 suppressed the elongated-mesocotyl phenotypes of d14l and d3 OsSMAX1 localizes to the nucleus and interacts with TOPLESS-RELATED PROTEINs, regulating downstream gene expression. Moreover, we showed that the GR24 enantiomers GR245DS and GR24 ent-5DS specifically inhibit mesocotyl elongation and regulate downstream gene expression in a D14- and D14L-dependent manner, respectively. Our work revealed that karrikin and SL signaling play parallel and additive roles in modulating downstream gene expression and negatively regulating mesocotyl elongation in the dark.

Identification of BBX proteins as rate-limiting cofactors of HY5.

As a source of both energy and environmental information, monitoring of incoming light is crucial for plants to optimize growth throughout development1. Concordantly, the light signalling pathways in plants are highly integrated with numerous other regulatory pathways2,3. One of these signal integrators is the basic leucine zipper domain (bZIP) transcription factor LONG HYPOCOTYL 5 (HY5), which has a key role as a positive regulator of light signalling in plants4,5. Although HY5 is thought to act as a DNA-binding transcriptional regulator6,7, the lack of any apparent transactivation domain8 makes it unclear how HY5 is able to accomplish its many functions. Here we describe the identification of three B-box containing proteins (BBX20, BBX21 and BBX22) as essential partners for HY5-dependent modulation of hypocotyl elongation, anthocyanin accumulation and transcriptional regulation. The bbx20 bbx21 bbx22 (bbx202122) triple mutant mimics the phenotypes of hy5 in the light and its ability to suppress the cop1 mutant phenotype in darkness. Furthermore, 84% of genes that exhibit differential expression in bbx202122 are also regulated by HY5, and we provide evidence that HY5 requires the B-box proteins for transcriptional regulation. Finally, expression of a truncated dark-stable version of HY5 (HY5(ΔN77)) together with BBX21 mutated in its VP motif strongly promoted de-etiolation in dark-grown seedlings, demonstrating the functional interdependence of these factors. In sum, this work clarifies long-standing questions regarding HY5 action and provides an example of how a master regulator might gain both specificity and dynamicity through the obligate dependence of cofactors.

Cdk9 and H2Bub1 signal to Clr6-CII/Rpd3S to suppress aberrant antisense transcription.

Mono-ubiquitylation of histone H2B (H2Bub1) and phosphorylation of elongation factor Spt5 by cyclin-dependent kinase 9 (Cdk9) occur during transcription by RNA polymerase II (RNAPII), and are mutually dependent in fission yeast. It remained unclear whether Cdk9 and H2Bub1 cooperate to regulate the expression of individual genes. Here, we show that Cdk9 inhibition or H2Bub1 loss induces intragenic antisense transcription of ∼10% of fission yeast genes, with each perturbation affecting largely distinct subsets; ablation of both pathways de-represses antisense transcription of over half the genome. H2Bub1 and phospho-Spt5 have similar genome-wide distributions; both modifications are enriched, and directly proportional to each other, in coding regions, and decrease abruptly around the cleavage and polyadenylation signal (CPS). Cdk9-dependence of antisense suppression at specific genes correlates with high H2Bub1 occupancy, and with promoter-proximal RNAPII pausing. Genetic interactions link Cdk9, H2Bub1 and the histone deacetylase Clr6-CII, while combined Cdk9 inhibition and H2Bub1 loss impair Clr6-CII recruitment to chromatin and lead to decreased occupancy and increased acetylation of histones within gene coding regions. These results uncover novel interactions between co-transcriptional histone modification pathways, which link regulation of RNAPII transcription elongation to suppression of aberrant initiation.

The photoperiodic response of hypocotyl elongation involves regulation of CDF1 and CDF5 activity.

Hypocotyl elongation relies on directional cell expansion, a process under light and circadian clock control. Under short photoperiods (SD), hypocotyl elongation in Arabidopsis thaliana follows a rhythmic pattern, a process in which circadian morning-to-midnight waves of the transcriptional repressors PSEUDO-RESPONSE REGULATORS (PRRs) jointly gate PHYTOCHROME-INTERACTING FACTOR (PIF) activity to dawn. Previously, we described CYCLING DOF FACTOR 5 (CDF5) as a target of this antagonistic PRR/PIF dynamic interplay. Under SD, PIFs induce CDF5 accumulation specifically at dawn, when it promotes the expression of positive cell elongation regulators such as YUCCA8 to induce growth. In contrast to SD, hypocotyl elongation under long days (LD) is largely reduced. Here, we examine whether CDF5 is an actor in this photoperiod specific regulation. We report that transcription of CDF5 is robustly induced in SD compared to LD, in accordance with PIFs accumulating to higher levels in SD, and in contrast to other members of the CDF family, whose expression is mainly clock regulated and have similar waveforms in SD and LD. Notably, when CDF5 was constitutively expressed under LD, CDF5 protein accumulated to levels comparable to SD but was inactive in promoting cell elongation. Similar results were observed for CDF1. Our findings indicate that both CDFs can promote cell elongation specifically in shorter photoperiods, however, their activity in LD is inhibited at the post-translational level. These data not only expand our understanding of the biological role of CDF transcription factors, but also identify a previously unrecognized regulatory layer in the photoperiodic response of hypocotyl elongation.

TEOSINTE BRANCHED1 regulates height and stem internode length in bread wheat.

Regulation of plant height and stem elongation has contributed significantly to improvement of cereal productivity by reducing lodging and improving distribution of assimilates to the inflorescence and grain. In wheat, genetic control of height has been largely contributed by the Reduced height-1 alleles that confer gibberellin insensitivity; the beneficial effects of these alleles are associated with less favourable effects involving seedling emergence, grain quality, and inflorescence architecture that have driven new research investigating genetic variation of stem growth. Here, we show that TEOSINTE BRANCHED1 (TB1) regulates height of wheat, with TB1 being expressed at low levels in nodes of the main culm prior to elongation, and increased dosage of TB1 restricting elongation of stem internodes. The effect of TB1 on stem growth is not accompanied by poor seedling emergence, as transgenic lines with increased activity of TB1 form longer coleoptiles than null transgenic controls. Analysis of height in a multiparent mapping population also showed that allelic variation for TB1 on the B genome influences height, with plants containing the variant TB-B1b allele being taller than those with the wild-type TB-B1a allele. Our results show that TB1 restricts height and stem elongation in wheat, suggesting that variant alleles that alter the expression or function of TB1 could be used as a new source of genetic diversity for optimizing architecture of wheat in breeding programmes.

Spanish spelt is unique germplasm for improvement of root hair length in hexaploid wheat

Longer root hair length (RHL) increases root surface area, thereby contributing to increased phosphorous uptake. This study aimed to identify useful germplasms and quantitative trait loci (QTL) for RHL improvement in wheat. The genetic variation in RHL was examined using hydroponic culture in 117 hexaploid wheat strains. Rhizosheath size and phosphorous uptake ability were also examined using high P-fixing soils with extremely low phosphorous availability (Andisols). QTL analysis was performed using backcross inbred lines from a cross between a Spanish spelt strain and a bread wheat variety. A wide range in genetic variation was found, especially in spelt wheat and landraces of bread wheat, whereas modern bread wheat varieties tended to show shorter RHL. Interestingly, remarkably longer RHL were observed in Spanish spelt strains than in strains from other countries. RHL exhibited a significant positive correlation with rhizosheath size and phosphorous uptake in soils. A QTL on chromosome 2A (QRhl.obu-2A) conferring longer RHL by the allele of a Spanish spelt strain was identified. It was co-located with TaRSL4-2AS, a key regulator of root hair elongation. Spanish spelt wheat strains could be unique germplasms that provide a useful allele for increasing RHL to enhance phosphorous uptake ability.

Gibberellin Signaling in Plants: Entry of a new MicroRNA Player.

GAs are essential hormones that control plant development as major regulators of stem elongation, germination, dormancy, flowering, leaf senescence, and fruit development ([Hedden and Thomas, 2012][1]). Their biosynthesis and signaling pathways are well established; however, the regulatory networks

Quantitative phosphoproteomics analysis reveals that protein modification and sugar metabolism contribute to sprouting in potato after BR treatment

Brassinosteroids (BRs), a new class of steroid hormones, are involved in the regulation of plant cell elongation and seed germination. Nevertheless, the molecular mechanism of the effect of BRs on tuber sprouting remains largely unknown. In this study, quantitative phosphoproteomics was employed to investigate the protein phosphorylation changes in sprouting induced by BRs. Our results showed that BRs accelerated the conversion of starch into soluble sugar in tubers. A functional enrichment cluster analysis suggested that the “amino acid metabolism pathway” was upregulated and that “plant hormone signal transduction and protein export” were downregulated. BR treatment also changed the phosphorylation of proteins involved in the BR, ABA, starch and sugar signal transduction pathways, such as serine/threonine-protein kinase (BSK), 14-3-3, alpha-glucan water dikinase (GWD), sucrose-phosphate synthase (SPS), sucrose synthase (SS) and alkaline/neutral invertase (A/N-INV). These results shed more light on the pattern of protein phosphorylation in BR promoting potato sprouting.

Prolonged mitosis results in structurally aberrant and over-elongated centrioles.

Centrioles are precisely built microtubule-based structures that assemble centrosomes and cilia. Aberrations in centriole structure are common in tumors, yet how these aberrations arise is unknown. Analysis of centriole structure is difficult because it requires demanding electron microscopy. Here we employ expansion microscopy to study the origins of centriole structural aberrations in large populations of human cells. We discover that centrioles do not have an elongation monitoring mechanism, which renders them prone to over-elongation, especially during prolonged mitosis induced by various factors, importantly including supernumerary centrioles. We identify that mitotic centriole over-elongation is dependent on mitotic Polo-like kinase 1, which we uncover as a novel regulator of centriole elongation in human cycling cells. While insufficient Plk1 levels lead to the formation of shorter centrioles lacking a full set of microtubule triplets, its overactivity results in over-elongated and structurally aberrant centrioles. Our data help explain the origin of structurally aberrant centrioles and why centriole numerical and structural defects coexist in tumors.

The DELLA proteins interact with MYB21 and MYB24 to regulate filament elongation in Arabidopsis

BackgroundGibberellin (GA) and jasmonate (JA) are two essential phytohormones for filament elongation in Arabidopsis. GA and JA trigger degradation of DELLAs and JASMONATE ZIM-domain (JAZ) proteins through SCFSLY1 and SCFCOI1 separately to activate filament elongation. In JA pathway, JAZs interact with MYB21 and MYB24 to control filament elongation. However, little is known how DELLAs regulate filament elongation.ResultsHere we showed that DELLAs interact with MYB21 and MYB24, and that R2R3 domains of MYB21 and MYB24 are responsible for interaction with DELLAs. Furthermore, we demonstrated that DELLA and JAZ proteins coordinately repress the transcriptional function of MYB21 and MYB24 to inhibit filament elongation.ConclusionWe discovered that DELLAs interact with MYB21 and MYB24, and that DELLAs and JAZs attenuate the transcriptional function of MYB21 and MYB24 to control filament elongation. This study reveals a novel cross-talk mechanism of GA and JA in the regulation of filament elongation in Arabidopsis.

SPEN integrates transcriptional and epigenetic control of X-inactivation

SummaryXist represents a paradigm for long non-coding RNA function in epigenetic regulation, although how it mediates X-chromosome inactivation (XCI) remains largely unexplained. Multiple Xist-RNA binding proteins have recently been identified, including SPEN1–3, the loss of which has been associated with deficient XCI at multiple loci2–6. Here we demonstrate that SPEN is a key orchestrator of XCI in vivo and unravel its mechanism of action. We show that SPEN is essential for initiating gene silencing on the X chromosome in preimplantation mouse embryos and embryonic stem cells. SPEN is dispensable for maintenance of XCI in neural progenitors, although it significantly dampens expression of genes that escape XCI. We show that SPEN is immediately recruited to the X-chromosome upon Xist up-regulation, and is targeted to enhancers and promoters of active genes. SPEN rapidly disengages from chromatin upon gene silencing, implying a need for active transcription to tether it to chromatin. We define SPEN’s SPOC domain as a major effector of SPEN’s gene silencing function, and show that tethering SPOC to Xist RNA is sufficient to mediate gene silencing. We identify SPOC’s protein partners which include NCOR/SMRT, the m6A RNA methylation machinery, the NuRD complex, RNA polymerase II and factors involved in regulation of transcription initiation and elongation. We propose that SPEN acts as a molecular integrator for initiation of XCI, bridging Xist RNA with the transcription machinery as well as nucleosome remodelers and histone deacetylases, at active enhancers and promoters.

Structural Basis of 7SK RNA 5′-Gamma-Phosphate Methylation and Retention by MePCE

7SK non-coding RNA is an essential regulator of eukaryotic transcription elongation through dynamic RNP assemblies that sequester or release the positive transcription elongation factor b (P-TEFb). All 7SK RNPs include a core comprising 7SK RNA, methylphosphate capping enzyme (MePCE), and La-related protein 7 (Larp7). In addition to its non-enzymatic role as a core component of 7SK RNPs, MePCE catalyzes the formation of a gamma-phosphate monomethylation cap, unique to 7SK and U6 in humans. How MePCE can specifically recognize and modify its RNA substrate and remain bound to 7SK to form the core 7SK RNP has not been previously known. We report 2.0 and 2.1 Å X-ray crystal structures of human MePCE methyltransferase domain bound to S-adenosylhomocysteine (SAH) and uncapped or capped 7SK substrates, respectively. We find that 7SK recognition is achieved by an extensive network of protein contacts to a 5' hairpin-single-stranded RNA region, involving the triphosphate group, two terminal basepairs and six single-stranded nucleotides, thus explaining MePCE specificity for 7SK and U6. The large size of the RNA binding site required for recognition and catalysis is unique among RNA methyltransferases studied to date. The structures reveal SAH and product RNA in a near-transition state geometry, where the cofactor SAH is buried inside the active site by the RNA-interacting residues. Unexpectedly, binding experiments show that MePCE has higher affinity for capped vs uncapped 7SK, with kinetic data supporting a slow product release model. Taken together, these data describe the features of an unusual RNA capping enzyme, and reveal the molecular mechanism of methyl transfer and 7SK retention by MePCE for subsequent assembly of the core 7SK RNP.

Adhesion G-protein-coupled receptor, GPR56, is required for Müllerian duct development in the chick.

The embryonic Müllerian ducts give rise to the female reproductive tract (fallopian tubes, uterus and upper vagina in humans, the oviducts in birds). Embryonic Müllerian ducts initially develop in both sexes, but later regress in males under the influence of anti-Müllerian hormone. While the molecular and endocrine control of duct regression in males have been well studied, early development of the ducts in both sexes is less well understood. Here, we describe a novel role for the adhesion G protein-coupled receptor, GPR56, in development of the Müllerian ducts in the chicken embryo. GPR56 is expressed in the ducts of both sexes from early stages. The mRNA is present during the elongation phase of duct formation, and it is restricted to the inner Müllerian duct epithelium. The putative ligand, Collagen III, is abundantly expressed in the Müllerian duct at the same developmental stages. Knockdown of GPR56 expression using in ovo electroporation results in variably truncated ducts, with a loss of expression of both epithelial and mesenchymal markers of duct development. Over-expression of GPR56 in vitro results in enhanced cell proliferation and cell migration. These results show that GPR56 plays an essential role in avian Müllerian duct development through the regulation of duct elongation.

Interrogation of the cell wall integrity pathway in Aspergillus niger identifies a putative negative regulator of transcription involved in chitin deposition.

Post-fermentation fungal biomass waste provides a viable source for chitin. Cell wall chitin of filamentous fungi, and in particular its de-N-acetylated derivative chitosan, has a wide range of commercial applications. Although the cell wall of filamentous fungi comprises 10–30% chitin, these yields are too low for cost-effective production. Therefore, we aimed to identify the genes involved in increased chitin deposition by screening a collection of UV-derived cell wall mutants in Aspergillus niger. This screen revealed a mutant strain (RD15.4#55) that showed a 30–40% increase in cell wall chitin compared to the wild type. In addition to the cell wall chitin phenotype, this strain also exhibited sensitivity to SDS and produces an unknown yellow pigment. Genome sequencing combined with classical genetic linkage analysis identified two mutated genes on chromosome VII that were linked with the mutant phenotype. Single gene knockouts and subsequent complementation analysis revealed that an 8 bp deletion in NRRL3_09595 is solely responsible for the associated phenotypes of RD15.4#55. The mutated gene, which was named cwcA (cell wall chitin A), encodes an orthologue of Saccharomyces cerevisiae Bypass of ESS1 (BYE1), a negative regulator of transcription elongation. We propose that this conserved fungal protein is involved in preventing cell wall integrity signaling under non-inducing conditions, where loss of function results in constitutive activation of the cell wall stress response pathway, and consequently leads to increased chitin content in the mutant cell wall.

FAK-Dependent Cell Motility and Cell Elongation.

Fibroblastic cells show specific substrate selectivity for typical cell–substrate adhesion. However, focal adhesion kinase (FAK) contributes to controlling the regulation of orientation and polarity. When fibroblasts attach to micropatterns, tyrosine-phosphorylated proteins and FAK are both detected along the inner border between the adhesive micropatterns and the nonadhesive glass surface. FAK likely plays important roles in regulation of cell adhesion to the substrate, as FAK is a tyrosine-phosphorylated protein that acts as a signal transduction molecule at sites of cell–substrate attachment, called focal adhesions. FAK has been suggested to play a role in the attachment of cells at adhesive micropatterns by affecting cell polarity. Therefore, the localization of FAK might play a key role in recognition of the border of the cell with the adhesive micropattern, thus regulating cell polarity and the cell axis. This review discusses the regulation and molecular mechanism of cell proliferation and cell elongation by FAK and its associated signal transduction proteins.

Dissecting the functional pleiotropism of lysine demethylase 5B in physiology and pathology

Background: The last two decades has been characterized by accruing evidence of the translational relevance of chromatin modification in normal genomic function, regulation, and pathology, especially with piqued interest in the intrinsic regulatory dynamism of histone methylation, and the increasing documentation of new members of the histone demethylase family. Recent studies provide functional and mechanistic insight into the peculiar biological role of these histone demethylases and their putative implication in pathological processes. Objective: This review aims to provide a summary of the latest findings related to pleiotropic roles of the Jumonji/AT-rich interactive domain (JARID) domain-containing lysine demethylase 5B (KDM5B, also known as JARID1B or PLU1) in physiology and pathology, with a focus on its therapeutic potentials. Results: KDM5B/JARID1B/PLU1 is restrictively expressed, evolutionarily conserved across mammalian species, and belonging to the α-ketoglutarate-dependent hydroxylase superfamily. KDM5B is actively involved in various physiological processes, including regulation of transcription elongation and alternative splicing in embryonic stem cells, epigenetic modulation of gene expression, neurogenesis, mammary gland development, and osteogenesis. Conversely, KDM5B is one of the earliest identified histone lysine demethylases associated with human disease, with several studies indicating that KDM5B plays a vital role in the initiation and progression of various malignancies, including lung, hypopharynx, brain, and breast cancers. Conclusion: This study provides concise insight into the functional pleiotropism of KDM5B in physiology and pathology, as well as highlights it role as an actionable therapeutic target.

Harmine enhances the activity of the HIV-1 latency-reversing agents ingenol A and SAHA.

ABSTRACTInfection with human immunodeficiency virus 1 (HIV-1) remains incurable because long-lived, latently-infected cells persist during prolonged antiretroviral therapy. Attempts to pharmacologically reactivate and purge the latent reservoir with latency reactivating agents (LRAs) such as protein kinase C (PKC) agonists (e.g. ingenol A) or histone deacetylase (HDAC) inhibitors (e.g. SAHA) have shown promising but incomplete efficacy. Using the J-Lat T cell model of HIV latency, we found that the plant-derived compound harmine enhanced the efficacy of existing PKC agonist LRAs in reactivating latently-infected cells. Treatment with harmine increased not only the number of reactivated cells but also increased HIV transcription and protein expression on a per-cell basis. Importantly, we observed a synergistic effect when harmine was used in combination with ingenol A and the HDAC inhibitor SAHA. An investigation into the mechanism revealed that harmine, when used with LRAs, increased the activity of NFκB, MAPK p38, and ERK1/2. Harmine treatment also resulted in reduced expression of HEXIM1, a negative regulator of transcriptional elongation. Thus, harmine enhanced the effects of LRAs by increasing the availability of transcription factors needed for HIV reactivation and promoting transcriptional elongation. Combination therapies with harmine and LRAs could benefit patients by achieving deeper reactivation of the latent pool of HIV provirus.

Pectate lyase-like Gene GhPEL76 regulates organ elongation in Arabidopsis and fiber elongation in cotton

Pectate lyases (PELs) play important roles in plant growth and development, mainly by degrading the pectin in primary cell walls. However, the role of PELs in cotton fiber elongation, which also involves changes in cellular structure and components, is poorly understood. Therefore, we aimed to isolate and characterize GhPEL76, as we suspected it to contribute to the regulation of fiber elongation. Expression analysis (qRT-PCR) revealed that GhPEL76 is predominately expressed in cotton fiber, with significantly different expression levels in long- and short-fiber cultivars, and that GhPEL76 expression is responsive to gibberellic acid and indoleacetic acid treatment. Furthermore, GhPEL76 promoter-driven β-glucuronidase activity was detected in the roots, hypocotyls, and leaves of transgenic Arabidopsis plants, and the overexpression of GhPEL76 in transgenic Arabidopsis promoted the elongation of several organs, including petioles, hypocotyls, primary roots, and trichomes. Additionally, the virus-induced silencing of GhPEL76 in cotton reduced fiber length, and both yeast one-hybrid and transient dual-luciferase assays suggested that GhbHLH13, a bHLH transcription factor that is up-regulated during fiber elongation, activates GhPEL76 expression by binding to the G-box of the GhPEL76 promoter region. Therefore, these results suggest GhPEL76 positively regulates fiber elongation and provide a basis for future studies of cotton fiber development.

Sub-toxic levels of Co2+ are anti-inflammatory and protect cartilage from degradation caused by IL-1β

BackgroundCobalt ions from some orthopaedic implants induce a dose-dependent cytotoxic and pro-inflammatory response. Recent studies show that sub-toxic levels of cobalt influence actin organisation regulating fibroblasts and macrophages behaviour. However little is known about the influence of sub-toxic levels of cobalt on articular cartilage biology and biomechanics. Previously, we have reported that IL-1β signalling in chondrocytes, is regulated by primary cilia and associated intraflagellar transport. Since primary cilia expression is modulated by actin organisation, we set out to test the hypothesis that sub-toxic levels of cobalt regulate cilia expression and IL-1β signalling thereby influencing articular cartilage degradation. MethodsIsolated chondrocytes and bovine cartilage explants were subjected to Co2+ in the presence and absence of IL-1β. Primary cilia were monitored by confocal immunofluorescence. Nitric oxide and PGE2 release were used to monitor IL-1β signalling. Degradation of cartilage matrix was assessed by the release of sGAG and the biomechanical properties of the tissue in uniaxial unconfined compression. FindingsSub-toxic levels of Co2+ (50 μM) blocked IL-1β-induced primary cilia elongation in isolated chondrocytes. This was associated with disruption of pro-inflammatory signalling in both isolated chondrocytes and cartilage explants, and inhibition of cartilage matrix degradation and loss of biomechanical properties. InterpretationThis study reveals that low levels of cobalt ions are anti-inflammatory, preventing cartilage degradation in response to IL-1β. This mechanism is associated with regulation of primary cilia elongation. These observations provide new insight into the potential beneficial role of cobalt and may lead to novel mechanisms for controlling cartilage inflammation.

An atypical HLH transcriptional regulator plays a novel and important role in strawberry ripened receptacle

BackgroundIn soft fruits, the differential expression of many genes during development and ripening is responsible for changing their organoleptic properties. In strawberry fruit, although some genes involved in the metabolic regulation of the ripening process have been functionally characterized, some of the most studied genes correspond to transcription factors. High throughput transcriptomics analyses performed in strawberry red receptacle (Fragaria x ananassa) allowed us to identify a ripening-related gene that codes an atypical HLH (FaPRE1) with high sequence homology with the PACLOBUTRAZOL RESISTANCE (PRE) genes. PRE genes are atypical bHLH proteins characterized by the lack of a DNA-binding domain and whose function has been linked to the regulation of cell elongation processes.ResultsFaPRE1 sequence analysis indicates that this gene belongs to the subfamily of atypical bHLHs that also includes ILI-1 from rice, SlPRE2 from tomato and AtPRE1 from Arabidopsis, which are involved in transcriptional regulatory processes as repressors, through the blockage by heterodimerization of bHLH transcription factors. FaPRE1 presented a transcriptional model characteristic of a ripening-related gene with receptacle-specific expression, being repressed by auxins and activated by abscisic acid (ABA). However, its expression was not affected by gibberellic acid (GA3). On the other hand, the transitory silencing of FaPRE1 transcription by agroinfiltration in receptacle produced the down-regulation of a group of genes related to the ripening process while inducing the transcription of genes involved in receptacle growth and development.ConclusionsIn summary, this work presents for the first time experimental data that support an important novel function for the atypical HLH FaPRE1 during the strawberry fruit ripening. We hypothesize that FaPRE1 modulates antagonistically the transcription of genes related to both receptacle growth and ripening. Thus, FaPRE1 would repress the expression of receptacle growth promoting genes in the ripened receptacle, while it would activate the expression of those genes related to the receptacle ripening process.