A DELAY OF GERMINATION 1 (DOG1)-like protein regulates spore germination in the moss Physcomitrium patens.

DELAY OF GERMINATION 1 is a key regulator of dormancy in flowering plants before seed germination. Bryophytes develop haploid spores with an analogous function to seeds. Here, we investigate whether DOG1 function during germination is conserved between bryophytes and flowering plants and analyse the underlying mechanism of DOG1 action in the moss Physcomitrium patens. Phylogenetic and in silico expression analyses were performed to identify and characterise DOG1 domain-containing genes in P. patens. Germination assays were performed to characterise a Ppdog1-like1 mutant, and replacement with AtDOG1 was carried out. Yeast two-hybrid assays were used to test the interaction of the PpDOG1-like protein with DELLA proteins from P. patens and A. thaliana. P. patens possesses nine DOG1 domain-containing genes. The DOG1-like protein PpDOG1-L1 (Pp3c3_9650) interacts with PpDELLAa and PpDELLAb and the A. thaliana DELLA protein AtRGA in yeast. Protein truncations revealed the DOG1 domain as necessary and sufficient for interaction with PpDELLA proteins. Spores of Ppdog1-l1 mutant germinate faster than wild type, but replacement with AtDOG1 reverses this effect. Our data demonstrate a role for the PpDOG1-LIKE1 protein in moss spore germination, possibly alongside PpDELLAs. This suggests a conserved DOG1 domain function in germination, albeit with differential adaptation of regulatory networks in seed and spore germination.

The Arabidopsis pre-mRNA 3' end processing related protein FIP1 promotes seed dormancy via the DOG1 and ABA pathways.

Seed dormancy is an important adaptive trait to prevent germination occurring at an inappropriate time. The mechanisms governing seed dormancy and germination are complex. Here, we report that FACTOR INTERACTING WITH POLY(A) POLYMERASE 1 (FIP1), a component of the pre-mRNA 3' end processing machinery, is involved in seed dormancy and germination processes in Arabidopsis thaliana. FIP1 is mainly expressed in seeds and the knockout of FIP1 causes reduced seed dormancy, indicating that FIP1 positively influences seed dormancy. Meanwhile, fip1 mutants are insensitive to exogenous ABA during seed germination and early seedling establishment. The terms 'seed maturation' and 'response to ABA stimulus' are significantly enriched in a gene ontology analysis based on genes differentially expressed between fip1-1 and the wild type. Several of these genes, including ABI5, DOG1 and PYL12, show significantly decreased transcript levels in fip1. Genetic analysis showed that either cyp707a2 or dog1-5 partially, but in combination completely, represses the reduced seed dormancy of fip1, indicating that the double mutant cyp707a2 dog1-5 is epistatic to fip1. Moreover, FIP1 is required for CFIM59, another component of pre-mRNA 3' end processing machinery, to govern seed dormancy and germination. Overall, we identified FIP1 as a regulator of seed dormancy and germination that plays a crucial role in governing these processes through the DOG1 and ABA pathways.

Complex control of seed germination timing by ERF50 involves RGL2 antagonism and negative feedback regulation of DOG1.

Seed dormancy governs germination timing, with both evolutionary and applied consequences. Despite extensive studies on the hormonal and genetic control of these processes, molecular mechanisms directly linking dormancy and germination remain poorly understood. By screening a collection of lines overexpressing Arabidopsis transcription factors, we identified ERF50 as a key gene to control dormancy and germination. To study its regulation, we measured seed-related physiological parameters in loss-of-function mutants and carried out transactivation, protein interaction and ChIP-PCR analyses. We found direct ERF50-mediated repression of DOG1 and activation of EXPA2 transcription, which results in enhanced seed germination. Although ERF50 expression is increased by DOG1 in dormant seeds, ERF50 germination-promoting activity is blocked by RGL2. The physiological, genetic and molecular evidence gathered here supports that ERF50 controls germination timing by regulating DOG1 levels to leverage its role as enhancer of seed germination, via RGL2 antagonism on EXPA2 expression. Our results highlight the central role of ERF50 as a feedback regulator to couple and fine-tune seed dormancy and germination.

Genome-wide identification of Avicennia marina aquaporins reveals their role in adaptation to intertidal habitats and their relevance to salt secretion and vivipary.

Aquaporins (AQPs) regulate the transport of water and other substrates, aiding plants in adapting to stressful environments. However, the knowledge of AQPs in salt-secreting and viviparous Avicennia marina is limited. In this study, 46 AmAQPs were identified in A. marina genome, and their subcellular localisation and function in transporting H2 O2 and boron were assessed through bioinformatics analysis and yeast transformation. Through analysing their expression patterns via RNAseq and real-time quantitative polymerase chain reaction, we found that most AmAQPs were downregulated in response to salt and tidal flooding. AmPIP (1;1, 1;7, 2;8, 2;9) and AmTIP (1;5, 1;6) as salt-tolerant candidate genes may contribute to salt secretion together with Na+ /H+ antiporters. AmPIP2;1 and AmTIP1;5 were upregulated during tidal flooding and may be regulated by anaerobic-responsive element and ethylene-responsive element cis-elements, aiding in adaptation to tidal inundation. Additionally, we found that the loss of the seed desiccation and dormancy-related TIP3 gene, and the loss of the seed dormancy regulator DOG1 gene, or DOG1 protein lack heme-binding capacity, may be genetic factors contributing to vivipary. Our findings shed light on the role of AQPs in A. marina adaptation to intertidal environments and their relevance to salt secretion and vivipary.

Regulation of seed dormancy by histone post-translational modifications in the model plant Arabidopsis thaliana.

Plants synchronize their growth and development with environmental changes, which is critical for their survival. Among their life cycle transitions, seed germination is key for ensuring the survival and optimal growth of the next generation. However, even under favorable conditions, often germination can be blocked by seed dormancy, a regulatory multilayered checkpoint integrating internal and external signals. Intricate genetic and epigenetic mechanisms underlie seed dormancy establishment, maintenance, and release. In this review, we focus on recent advances that shed light on the complex mechanisms associated with physiological dormancy, prevalent in seed plants, with Arabidopsis thaliana serving as a model. Here, we summarize the role of multiple epigenetic regulators, but with a focus on histone modifications such as acetylation and methylation, that finely tune dormancy responses and influence dormancy-associated gene expression. Understanding these mechanisms can lead to a better understanding of seed biology in general, as well as resulting in the identification of possible targets for breeding climate-resilient plants.

Primary EGIST of the greater omentum - a rare presentation.

Extragastrointestinal stromal tumors (EGISTs) are rare mesenchymal neoplasms, which develop in the retroperitoneum, mesentery, and omentum, lacking continuity to the stomach or intestines. Authors hereby present a female patient with a large heterogeneous abdominal mass as a case of an omental EGIST. A 46-year-old woman was referred to our hospital due to an insidious enlargement and colicky pain in the right iliac fossa. Abdominal palpation revealed a voluminous, freely mobile, and non-pulsatile mesoabdominal bulge expanding to the hypogastrium. On exploratory midline laparotomy, the tumor was densely fused to the greater omentum, not connected to the stomach, without gross involvement of adjacent structures. The large mass was completely excised after adequate mobilization. Immunohistochemical techniques showed strong and diffuse expression of WT1, actin and DOG-1, as well as multifocal c-KIT marking. Mutational study concluded a double mutation of KIT exon 9 and a mutation of PDGFRA exon 18. The patient was submitted to adjuvant treatment with imatinib mesylate 800 mg/day. Despite an extremely diverse presentation, omental EGISTs often remain clinically silent for a long time having enough space to grow before becoming symptomatic. These tumors have a consistent pattern of metastasis that typically spares lymph nodes unlike epithelial gut neoplasms. Surgery remains the preferred treatment for non-metastatic EGISTs of the greater omentum. It is possible that DOG-1 will supplant KIT as the leading marker in the future. The scarcity of knowledge on omental EGISTs implies a close monitoring of these patients to detect local relapse or distant metastasis.

Seed dormancy 4 like1 of Arabidopsis is a key regulator of phase transition from embryo to vegetative development.

Seed dormancy is an adaptive trait that enables plants to survive adverse conditions and restart growth in a season and location suitable for vegetative and reproductive growth. Control of seed dormancy is also important for crop production and food quality because it can help induce uniform germination and prevent preharvest sprouting. Rice preharvest sprouting quantitative trait locus analysis has identified Seed dormancy 4 (Sdr4) as a positive regulator of dormancy development. Here, we analyzed the loss-of-function mutant of the Arabidopsis ortholog, Sdr4 Like1 (SFL1), and found that the sfl1-1 seeds showed precocious germination at the mid- to late-maturation stage similar to rice sdr4 mutant, but converted to become more dormant than the wild type during maturation drying. Coordinated with the dormancy levels, expression levels of the seed maturation and dormancy master regulator genes, ABI3, FUS3, and DOG1 in sfl1-1 seeds were lower than in wild type at early- and mid-maturation stages, but higher at the late-maturation stage. In addition to the seed dormancy phenotype, sfl1-1 seedlings showed a growth arrest phenotype and heterochronic expression of LAFL (LEC1, ABI3, FUS3, LEC2) and DOG1 in the seedlings. These data suggest that SFL1 is a positive regulator of initiation and termination of the seed dormancy program. We also found genetic interaction between SFL1 and the SFL2, SFL3, and SFL4 paralogs of SFL1, which impacts on the timing of the phase transition from embryo maturation to seedling growth.

A transcription factor WRKY36 interacts with AFP2 to break primary seed dormancy by progressively silencing DOG1 in Arabidopsis.

The phytohormones abscisic acid (ABA) and gibberellic acid (GA) antagonistically control the shift between seed dormancy and its alleviation. DELAY OF GERMINATION1 (DOG1) is a critical regulator that determines the intensity of primary seed dormancy, but its underlying regulatory mechanism is unclear. In this study, we combined physiological, biochemical, and genetic approaches to reveal that a bHLH transcriptional factor WRKY36 progressively silenced DOG1 expression to break seed dormancy through ABI5-BINDING PROTEIN 2 (AFP2) as the negative regulator of ABA signal. AFP2 interacted with WRKY36, which recognizes the W-BOX in the DOG1 promoter to suppress its expression; Overexpressing WRKY36 broke primary seed dormancy, whereas wrky36 mutants showed strong primary seed dormancy. In addition, AFP2 recruited the transcriptional corepressor TOPLESS-RELATED PROTEIN2 (TPR2) to reduce histone acetylation at the DOG1 locus, ultimately mediating WRKY36-dependent inhibition of DOG1 expression to break primary seed dormancy. Our result proposes that the WRKY36-AFP2-TPR2 module progressively silences DOG1 expression epigenetically, thereby fine-tuning primary seed dormancy.

Primary vulvar extragastrointestinal stromal tumor in a 77-year-old woman.

Extragastrointestinal stromal tumors (EGISTs) carry the same morphological, immunohistochemical and molecular features as gastrointestinal stromal tumors (GISTs) and involve extragastrointestinal tract soft tissue. The majority of reported EGIST cases arise from intraabdominal, retroperitoneal, or pelvic soft tissue. A significant subset of such tumors originates from the gastrointestinal muscle layer, grows in an exophytic manner, then loses attachment to the gastrointestinal tract. Consequently, true EGISTs are exceedingly rare. Herein, we are reporting a case of a vulvar EGIST. A 77-year-old woman presented with a painless subcutaneous nodule on the right perineum. An excisional biopsy showed a fairly circumscribed bland spindle cell lesion in the dermis. The tumor cells were positive for CD117 and ANO1/DOG-1 and negative for smooth muscle myosin, smooth muscle actin, STAT6, low- and high-molecular-weight cytokeratins, SOX10, MART-1, CD10, S-100 protein, and estrogen and progesterone receptors. A diagnosis of EGIST was made and complete excision was recommended. Superficial/subcutaneous EGISTs are extremely rare, and it is important for dermatopathologists to be aware of this entity as it can be misdiagnosed as more common spindle cell neoplasms, both benign and malignant, including but not limited to smooth muscle neoplasms (leiomyoma/leiomyosarcoma), spindle cell melanoma, and sarcomatoid squamous cell carcinoma.

Diagnosis of acinic cell carcinoma of the salivary gland on cytology specimens: Role of NOR-1 (NR4A3) immunohistochemistry.

OBJECTIVES: Acinic cell carcinoma (AcCC) is often a challenging diagnosis on cytology. Recently, NOR-1 (NR4A3) has been demonstrated as a sensitive and specific marker for AcCC. Therefore, we conducted this study to evaluate NOR-1 expression in AcCC cytology specimens and to compare its reactivity in other salivary gland tumours (non-AcCC). METHODS: We retrospectively reviewed our database and selected cytology cases with available cell blocks, including 10 AcCC and 24 non-AcCC tumours (12 benign tumours and 12 malignant tumours). NOR-1 (1:50 dilution; SC393902 [H-7]; Santa Cruz Biotech) immunohistochemistry (IHC) was performed on all cases. RESULTS: All AcCC cases except two (2/10, 80%) showed positive nuclear staining of variable intensity for NOR-1, with the majority of cases (75%) demonstrating at least moderately intense nuclear expression. All non-AcCC cases were negative for NOR-1, demonstrating a specificity of 100%. CONCLUSION: We conclude that NOR-1 IHC is sensitive and very specific on cytology specimens and is able to distinguish AcCC from its mimickers reliably and classify them appropriately for further management.

Utility of immunohistochemical expression of H3.3K36M and DOG1 in the diagnosis of chondroblastomas: An experience from a tertiary cancer referral center.

Despite its characteristic clinicopathological features, chondroblastoma may pose a diagnostic challenge, given its morphological spectrum, potential for subdiagnostic appearances in limited biopsy specimens, and its potential mimicry of other entities. Recently, a characteristic H3F3B mutation underlying most chondroblastomas was described, which led to the identification of H3.3K36M as the corresponding diagnostic immunohistochemical marker. The present study is an evaluation of immunohistochemical features of 26 chondroblastomas, including DOG1 and H3.3K36M immunostaining. H3.3K36M immunostaining was graded as 1+, 2+ and 3+ in terms of staining intensity. There were 17 males and 9 females (M:F = 1.8:1) with ages ranging from 7 to 34 years (average = 16.7, median = 16). The most common location was proximal humerus (8, 30.7 %) followed by proximal tibia (5, 19.2 %), distal femur (3, 11.5 %), proximal femur (3, 11.5 %), pelvis (2,), followed by distal tibia, calcaneum, upper sternum, scapula, and D9 vertebra, in a single case, respectively. Eighteen (69.23 %) tumors displayed all the classic histopathological features. Immunohistochemically, the tumor cells were positive for S-100 P (19/22, 86.3 %), DOG1 (focal to patchy) (21/23 91.3 %), and H3.3K36M (26/26, 100 %). H3.3K36M tested in other tumors, constituting diagnostic mimics of a chondroblastoma, such as giant cell tumor of bone, chondromyxoid fibroma, and tenosynovial giant cell tumors, showed negative staining. Six tumors, initially diagnosed as chondroblastomas were reclassified into other entities with the help of negative H3.3K36M immunostaining. The present study reinforces H3.3K36M as a highly sensitive and specific marker for diagnosing chondroblastoma, including small biopsies, and in uncommon tumor sites with variable histopathological features. DOG1 is also useful in reinforcing a diagnosis of chondroblastoma in a clinicoradiological context, especially in laboratories lacking H3.3K36M immunostain. However, its staining pattern is variable.

The SlDOG1 Affect Biosynthesis of Steroidal Glycoalkaloids by Regulating GAME Expression in Tomato.

Steroidal alkaloids (SAs) and steroidal glycoalkaloids (SGAs) are common constituents of plant species belonging to the Solanaceae family. However, the molecular mechanism regulating the formation of SAs and SGAs remains unknown. Here, genome-wide association mapping was used to elucidate SA and SGA regulation in tomatoes: a SlGAME5-like glycosyltransferase (Solyc10g085240) and the transcription factor SlDOG1 (Solyc10g085210) were significantly associated with steroidal alkaloid composition. In this study, it was found that rSlGAME5-like can catalyze a variety of substrates for glycosidation and can catalyze SA and flavonol pathways to form O-glucoside and O-galactoside in vitro. The overexpression of SlGAME5-like promoted α-tomatine, hydroxytomatine, and flavonol glycoside accumulation in tomatoes. Furthermore, assessments of natural variation combined with functional analyses identified SlDOG1 as a major determinant of tomato SGA content, which also promoted SA and SGA accumulation via the regulation of GAME gene expression. This study provides new insights into the regulatory mechanisms underlying SGA production in tomatoes.

Ectopic expression of the Arabidopsis florigen gene FLOWERING LOCUS T in seeds enhances seed dormancy via the GA and DOG1 pathways.

Ectopic expression of specific genes in seeds could be a tool for molecular design of crops to alter seed dormancy and germination, thereby improving production. Here, a seed-specific vector, 12S-pLEELA, was applied to study the roles of genes in Arabidopsis seeds. Transgenic lines containing FLOWERING LOCUS T (FT) driven by the 12S promoter exhibited significantly increased seed dormancy and earlier flowering. Mutated FT(Y85H) and TERMINAL FLOWER1 (TFL1) transgenic lines also showed increased seed dormancy but without altered flowering time. FT(Y85H) and TFL1 caused weaker seed dormancy enhancement compared to FT. The FT and TFL1 transgenic lines showed hypersensitivity to paclobutrazol, but not to abscisic acid in seed germination. The levels of bioactive gibberellin 3 (GA3 ) and GA4 were significantly reduced, consistent with decreased expression of COPALYL DIPHOSPHATE SYNTHASE (CPS), KAURENE OXIDASE (KO), GIBBERELLIN 3-OXIDASE2 (GA3ox2), and GA20ox1 in p12S::FT lines. Exogenous GA4+7 could recover the germination ability of FT transgenic lines. These results revealed that FT regulates GA biosynthesis. A genetic analysis indicated that the GA signaling regulator SPINDLY (SPY) is epistatic to FT in GA-mediated seed germination. Furthermore, DELAY OF GERMINATION1 (DOG1) showed significantly higher transcript levels in p12S::FT lines. Seed dormancy analysis of dog1-2 spy-3 p12S::FT-2 indicated that the combination of SPY and DOG1 is epistatic to FT in the regulation of dormancy. Overall, we showed that ectopic expression of FT and TFL1 in seeds enhances dormancy through affecting GA and DOG1 pathways.

DELAY OF GERMINATION 1, the Master Regulator of Seed Dormancy, Integrates the Regulatory Network of Phytohormones at the Transcriptional Level to Control Seed Dormancy.

Seed dormancy, an important adaptive trait that governs germination timing, is endogenously controlled by phytohormones and genetic factors. DELAY OF GERMINATION 1 (DOG1) is the vital genetic regulator of dormancy, significantly affecting the expression of numerous ABA and GA metabolic genes. However, whether DOG1 could influence the expression of other phytohormone-related genes is still unknown. Here, we comprehensively investigated all well-documented hormone-related genes which might be affected in dog1-2 dry or imbibed seeds by using whole-transcriptome sequencing (RNA-seq). We found that DOG1 could systematically control the expression of phytohormone-related genes. An evident decrease was observed in the endogenous signal intensity of abscisic acid (ABA) and indole-3-acetic acid (IAA), while a dramatic increase appeared in that of gibberellins (GA), brassinosteroids (BR), and cytokinin (CK) in the dog1-2 background, which may contribute considerably to its dormancy-deficient phenotype. Collectively, our data highlight the role of DOG1 in balancing the expression of phytohormone-related genes and provide inspirational evidence that DOG1 may integrate the phytohormones network to control seed dormancy.

Gastrointestinal stromal tumors with Kit gene mutation in 4 guinea pigs (Cavia porcellus).

Gastrointestinal stromal tumors (GISTs) have been rarely reported in guinea pigs. We aimed to characterize the clinical and pathological features of GISTs in 4 guinea pigs and investigate the presence of mutations in exon 11 of the KIT proto-oncogene receptor tyrosine kinase (Kit) gene. Two subjects were male and 2 were female; 2 were 6 years old, 1 was 7 years old, and 1 was of an unknown age. Three cases had primary gastric tumors, whereas 1 had a primary small intestinal tumor. All cases had tumors that extended from the submucosa to the serosa with extraluminal growth. A gastric tumor had gastric, pancreatic, and cecal metastases. Histologically, the tumors were sharply demarcated and composed of spindle cells arranged in bundles, intermixed with small amounts of collagenous stroma. The tumor cells had mild atypia with few mitotic figures (0-5/50 high power fields, 7.95 mm2) and were immunolabeled for KIT and Discovered-on-GIST 1 (DOG1). All cases had mutations in exon 11 of the Kit gene. These findings indicate that GISTs in guinea pigs are similar to those in humans and dogs. GISTs in guinea pigs are potentially malignant submucosal tumors with KIT- and DOG1-immunolabeling, exon 11 KIT mutations, and the possibility of metastasis.

DOG1 as an Immunohistochemical Marker of Acinic Cell Carcinoma: A Systematic Review and Meta-Analysis.

DOG1 is a transmembrane protein originally discovered on gastrointestinal stromal tumors and works as a calcium-activated chloride channel protein. There are a limited number of articles on the potential utility of this antibody in the diagnosis of salivary gland tumors in routine practice. In this study, we aimed to investigate the role of DOG1 as an immunohistochemical marker in patients with salivary acinic cell carcinoma (ACC) through meta-analysis. A literature search was performed of the PubMed, Scopus, and Web of Science databases for English-language studies published from January 2010 to September 2021. The literature search revealed 148 articles, of which 20 were included in the study. The overall rate of DOG1 expression in salivary acinic cell carcinoma was 55% (95% CI = 0.43-0.58). Although ACC is a challenging diagnosis, paying careful attention to the cytomorphological features in conjunction with DOG1 immunostaining can help to reach an accurate diagnosis.

DOG-1 positive primary acinic cell carcinoma of the lung and investigation of molecular status.

Primary acinic cell carcinoma (ACC) of the lung is an extremely rare neoplasm that more often arises near to a right bronchus. It is characterized by two populations of clear and dark eosinophilic cells, arranged in a glandular acinar pattern. Mitosis are rare and tumor cells show small and eccentric nuclei. Positive stain for PAS, PAS-D, cytokeratin, A1AT and A1ACT is reported, while TTF1, p40, synaptophysin, SMA, and S100 are substantially negative. DOG-1 positive stain was observed in ACC of the salivary glands and its negativity was proposed to distinguish between primary and metastatic ACC of the lung. Here, we report the 30th case of primary ACC of the lung, describing the immunohistochemical positivity for DOG-1 and the molecular status of the neoplasm for the first time.

Ancient and recent gene duplications as evolutionary drivers of the seed maturation regulators DELAY OF GERMINATION1 family genes.

The DELAY OF GERMINATION1 (DOG1) family genes (DFGs) in Arabidopsis thaliana are involved in seed dormancy, reserve accumulation, and desiccation tolerance. Decoding the molecular evolution of DFGs is key to understanding how these seed programs evolved. This article demonstrates that DFGs have diverged in the four lineages DOG1, DOG1-LIKE4 (DOGL4), DOGL5 and DOGL6, whereas DOGL1, DOGL2 and DOGL3 arose separately within the DOG1 lineage. The systematic DFG nomenclature proposed in this article addresses the current issues of inconsistent DFG annotation and highlights DFG genomic synteny in angiosperms. DFG pseudogenes, or collapsed coding sequences, hidden in the genomes of early-diverging angiosperms are documented here. They suggest ancient birth and loss of DFGs over the course of angiosperm evolution. The proposed models suggest that the origin of DFG diversification dates back to the most recent common ancestor of living angiosperms. The presence of a single form of DFG in nonflowering plants is discussed. Phylogenetic analysis of gymnosperm, lycophyte, and liverwort DFGs and similar genes found in mosses and algae suggests that DFGs diverged from the TGACG motif-binding transcription factor genes before the divergence of the bryophyte lineage.

Temperature during seed maturation controls seed vigour through ABA breakdown in the endosperm and causes a passive effect on DOG1 mRNA levels during entry into quiescence.

Temperature variation during seed set is an important modulator of seed dormancy and impacts the performance of crop seeds through effects on establishment rate. It remains unclear how changing temperature during maturation leads to dormancy and growth vigour differences in nondormant seedlings. Here we take advantage of the large seed size in Brassica oleracea to analyse effects of temperature on individual seed tissues. We show that warm temperature during seed maturation promotes seed germination, while removal of the endosperm from imbibed seeds abolishes temperature-driven effects on germination. We demonstrate that cool temperatures during early seed maturation lead to abscisic acid (ABA) retention specifically in the endosperm at desiccation. During this time temperature affects ABA dynamics in individual seed tissues and regulates ABA catabolism. We also show that warm-matured seeds preinduce a subset of germination-related programmes in the endosperm, whereas cold-matured seeds continue to store maturation-associated transcripts including DOG1 because of effects on mRNA degradation before quiescence, rather than because of the effect of temperature on transcription. We propose that effects of temperature on seed vigour are explained by endospermic ABA breakdown and the divergent relationships between temperature and mRNA breakdown and between temperature, seed moisture and the glass transition.

Trait analysis reveals DOG1 determines initial depth of seed dormancy, but not changes during dormancy cycling that result in seedling emergence timing.

Seedling emergence timing is crucial in competitive plant communities and so contributes to species fitness. To understand the mechanistic basis of variation in seedling emergence timing, we exploited the contrasting behaviour of two Arabidopsis thaliana ecotypes: Cape Verde Islands (Cvi) and Burren (Bur-0). We used RNA-Seq analysis of RNA from exhumed seeds and quantitative trait loci (QTL) analyses on a mapping population from crossing the Cvi and Bur-0 ecotypes. We determined genome-wide expression patterns over an annual dormancy cycle in both ecotypes, identifying nine major clusters based on the seasonal timing of gene expression, and variation in behaviour between them. QTL were identified for depth of seed dormancy and seedling emergence timing (SET). Both analyses showed a key role for DOG1 in determining depth of dormancy, but did not support a direct role for DOG1 in generating altered seasonal patterns of seedling emergence. The principle QTL determining SET (SET1: dormancy cycling) is physically close on chromosome 5, but is distinct from DOG1. We show that SET1 and two other SET QTLs each contain a candidate gene (AHG1, ANAC060, PDF1 respectively) closely associated with DOG1 and abscisic acid signalling and suggest a model for the control of SET in the field.