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Abstract Background Inflorescence architecture and floral development in flowering plants are determined by genetic control of meristem identity, determinacy, and maintenance. The ear inflorescence meristem in maize (Zea mays) initiates short branch meristems called spikelet pair meristems, thus unlike the tassel inflorescence, the ears lack long branches. Maize growth-regulating factor (GRF)-interacting factor1 (GIF1) regulates branching and size of meristems in the tassel inflorescence by binding to Unbranched3. However, the regulatory pathway of gif1 in ear meristems is relatively unknown. Result In this study, we found that loss-of-function gif1 mutants had highly branched ears, and these extra branches repeatedly produce more branches and florets with unfused carpels and an indeterminate floral apex. In addition, GIF1 interacted in vivo with nine GRFs, subunits of the SWI/SNF chromatin-remodeling complex, and hormone biosynthesis-related proteins. Furthermore, key meristem-determinacy gene RAMOSA2 (RA2) and CLAVATA signaling-related gene CLV3/ENDOSPERM SURROUNDING REGION (ESR) 4a (CLE4a) were directly bound and regulated by GIF1 in the ear inflorescence. Conclusions Our findings suggest that GIF1 working together with GRFs recruits SWI/SNF chromatin-remodeling ATPases to influence DNA accessibility in the regions that contain genes involved in hormone biosynthesis, meristem identity and determinacy, thus driving the fate of axillary meristems and floral organ primordia in the ear-inflorescence of maize.

Selection of kernel number per ear has improved maize yield, but the genetic base is unclear. Here, the authors reveal that a serine/threonine protein kinase KNR6 is a positive regulator of the trait and show in vitro evidences that KNR6 may function through phosphorylating an Arf GTPase-activating protein.

Enhancers are cis-acting DNA segments with the ability to increase target gene expression. They show high sensitivity to DNase and contain specific DNA elements in an open chromatin state that allows the binding of transcription factors (TFs). While numerous enhancers are annotated in the maize genome, few have been characterized genetically. KERNEL ROW NUMBER4 (KRN4), an intergenic quantitative trait locus for kernel row number, is assumed to be a cis-regulatory element of UNBRANCHED3 (UB3), a key inflorescence gene. However, the mechanism by which KRN4 controls UB3 expression remains unclear. Here, we found that KRN4 exhibits an open chromatin state, harboring sequences that showed high enhancer activity toward the 35S and UB3 promoters. KRN4 is bound by UB2-centered transcription complexes and interacts with the UB3 promoter by three duplex interactions to affect UB3 expression. Sequence variation at KRN4 enhances ub2 and ub3 mutant ear fasciation. Therefore, we suggest that KRN4 functions as a distal enhancer of the UB3 promoter via chromatin interactions and recruitment of UB2-centered transcription complexes for the fine-tuning of UB3 expression in meristems of ear inflorescences. These results provide evidence that an intergenic region helps to finely tune gene expression, providing a new perspective on the genetic control of quantitative traits.

The KERNEL NUMBER PER ROW6 (KNR6)-mediated phosphorylation of an adenosine diphosphate ribosylation factor (Arf) GTPase-activating protein (AGAP) forms a key regulatory module for the numbers of spikelets and kernels in the ear inflorescences of maize (Zea mays L.). However, the action mechanism of the KNR6–AGAP module remains poorly understood. Here, we characterized the AGAP-recruited complex and its roles in maize cellular physiology and agronomically important traits. AGAP and its two interacting Arf GTPase1 (ARF1) members preferentially localized to the Golgi apparatus. The loss-of-function AGAP mutant produced by CRISPR/Cas9 resulted in defective Golgi apparatus with thin and compact cisternae, together with delayed internalization and repressed vesicle agglomeration, leading to defective inflorescences and roots, and dwarfed plants with small leaves. The weak agap mutant was phenotypically similar to knr6, showing short ears with fewer kernels. AGAP interacted with KNR6, and a double mutant produced shorter inflorescence meristems and mature ears than the single agap and knr6 mutants. We hypothesized that the coordinated KNR6–AGAP–ARF1 complex modulates vegetative and reproductive traits by participating in vesicle trafficking in maize. Our findings provide a novel mechanistic insight into the regulation of inflorescence development, and ear length and kernel number, in maize.

Dairy production is an important source of nutrients in the global food supply, but environmental impacts are increasingly a concern of consumers, scientists, and policy-makers. Many decisions must be integrated to support sustainable production—which can be achieved using a simulation model. We provide an example of the Ruminant Farm Systems (RuFaS) model to assess changes in the dairy system related to altered animal feed efficiency. RuFaS is a whole-system farm simulation model that simulates the individual animal life cycle, production, and environmental impacts. We added a stochastic animal-level parameter to represent individual animal feed efficiency as a result of reduced residual feed intake and compared High (intake = 94% of expected) and Very High (intake = 88% of expected) efficiency levels with a Baseline scenario (intake = 100% of expected). As expected, the simulated total feed intake was reduced by 6 and 12% for the High and Very High efficiency scenarios, and the expected impact of these improved efficiencies on the greenhouse gas emissions from enteric methane and manure storage was a decrease of 4.6 and 9.3%, respectively.

Kernel row number (KRN) is an important component of yield during the domestication and improvement of maize and controlled by quantitative trait loci (QTL). Here, we fine-mapped a major KRN QTL, KRN4, which can enhance grain productivity by increasing KRN per ear. We found that a ~3-Kb intergenic region about 60 Kb downstream from the SBP-box gene Unbranched3 (UB3) was responsible for quantitative variation in KRN by regulating the level of UB3 expression. Within the 3-Kb region, the 1.2-Kb Presence-Absence variant was found to be strongly associated with quantitative variation in KRN in diverse maize inbred lines, and our results suggest that this 1.2-Kb transposon-containing insertion is likely responsible for increased KRN. A previously identified A/G SNP (S35, also known as Ser220Asn) in UB3 was also found to be significantly associated with KRN in our association-mapping panel. Although no visible genetic effect of S35 alone could be detected in our linkage mapping population, it was found to genetically interact with the 1.2-Kb PAV to modulate KRN. The KRN4 was under strong selection during maize domestication and the favorable allele for the 1.2-Kb PAV and S35 has been significantly enriched in modern maize improvement process. The favorable haplotype (Hap1) of 1.2-Kb-PAV-S35 was selected during temperate maize improvement, but is still rare in tropical and subtropical maize germplasm. The dissection of the KRN4 locus improves our understanding of the genetic basis of quantitative variation in complex traits in maize.