Biology subjects

Lee, S.-B.

Publications and source records attributed to Lee, S.-B..

6 recordsLinked to original sources

bioRxiv2024

Evolutionary unique N-glycan-dependent protein quality control system plays pivotal roles in cellular fitness and extracellular vesicle transport in Cryptococcus neoformans

A conserved N-glycan-dependent endoplasmic reticulum protein quality control (ERQC) system has evolved in eukaryotes to ensure accuracy during glycoprotein folding. The human pathogen Cryptococcus neoformans possesses a unique N-glycosylation pathway that affects microbial physiology and interactions with the infected host. To investigate the molecular features and functions of the ERQC system in C. neoformans, we characterized a set of mutants with deletion of genes coding for the ERQC sensor UDP-glucose:glycoprotein glucosyltransferase (UGG1) and putative 1,2-mannose-trimming enzymes (MNS1, MNS101, MNL1, and MNL2). The ugg1{Delta}, mns1{Delta}, mns101{Delta}, and mns1{Delta}101{Delta} mutants showed alterations in N-glycan profiles, defective cell surface organization, decreased survival in host cells, and varying degrees of reduced in vivo virulence. The ugg1{Delta} strain exhibited severely impaired extracellular secretion of capsular polysaccharides and virulence-related enzymes. Comparative transcriptome analysis showed the upregulation of protein folding, proteolysis, and cell wall remodeling genes, indicative of induced ER stress. However, no apparent changes were observed in the expression of genes involved in protein secretion or capsule biosynthesis. Additionally, extracellular vesicle (EV) analysis combined with proteomic analysis showed significant alterations in the number, size distribution, and cargo composition of EVs in ugg1{Delta}. These findings highlight the essential role of the functional ERQC system for cellular fitness under adverse conditions and proper EV-mediated transport of virulence factors, which are crucial for the full fungal pathogenicity of C. neoformans.

microbiology↗

bioRxiv2024

The strength of sexual signals predicts same-sex paring in termites

Same-sex sexual behavior (SSB) is an enigma in behavioral ecology as it does not result in reproduction. Proximately, the evolution of sexual signals is critical for the evolution of SSB in a sex-specific manner. For signal receivers, the loss of sexual signals leads to smaller phenotypic sex differences, leading to frequent accidental SSB between receivers. Alternatively, for senders, sexual signals could help locate another sender, enhancing intentional SSB as in heterosexual pairing. Here, we demonstrate this link between sex pheromone signaling and the frequency of same-sex pairing in two Coptotermes termites that use the same chemical as sex pheromones but in different quantities. In termites, mating pairs engage in tandem runs, where a male follows a female with sex pheromones. We found that female-female tandems were more stable in C. formosanus, whose females produce more pheromones, while the male-male interactions were more frequent in C. gestroi, whose females produce fewer pheromones. Thus, stronger pheromones lead to sender-sender SSB, while weaker pheromones lead to receiver-receiver SSB. In both species, same-sex tandems were less stable than heterosexual tandems, contrasting with Reticulitermes, another termite group that shows frequent same-sex tandems. The proximate mechanism of SSB is diverse, reflecting the heterosexual context.

animal behavior and cognition↗

bioRxiv2023

An ensemble of Gleditsia sinensis Lam. and gut microbiota against alcoholic liver disease

Gleditsia sinensis Lam. (GSL) is a medicinal herb and a noticeable resource of possessing hepatic protective agents such as alcoholic liver disease (ALD). At present, it has been documented that gut microbiota (GM) is related directly to etiology of ALD. Nevertheless, the bioactive molecules in GSL, favorable GM, targets, and key mechanism(s) against ALD are yet to be revealed. Hence, we integrated the significant four components to clarify the nuanced pathogenesis with help of network pharmacology (NP) concept. We retrieved significant metabolites via gutMGene and constructed GSL or GM-Signaling pathways-Targets-Metabolites (GGSTM) networks. Finally, molecular docking test (MDT) was performed to verify the key findings. The gutMGene suggested that 16 GM and 6 metabolites were related to the two signaling pathways through GGSTM networks. Both MDT and frontier molecular orbitals (FMO) theory revealed the most stable conformers: equol from Lactobacillus paracasei JS1 on IL6, Bauer-7-en-3-one, and Urs-12-en-3-one from GSL on PPARA, PPARD, and PPARG, respectively. In conclusion, this study sheds light on the combinatorial effects of GM, and GSL in treating ALD via systems biology concept.

systems biology↗

bioRxiv2021

Coordination of movement via complementary interactions of leaders and followers in termite mating pairs

Leadership of animal group movements depends on social feedback, hence leaders signals and followers responses should be attuned to each other. However, leader and follower roles are difficult to disentangle in species with high levels of coordination. To overcome this challenge, we investigated a simple case of movement coordination: termite pairs in which a female leads a male as they search for a nest site. To tease apart leader and follower roles, we created conspecific and heterospecific pairs of Coptotermes gestroi and C. formosanus, which share a pairing pheromone so that males follow females of either species. Conspecific pairs were stable for both species, even though C. gestroi females produce less pheromone than C. formosanus. Heterospecific pairs with C. gestroi males were also stable, but not those with C. formosanus males. We attributed this difference to the C. gestroi males unique capacity to follow females that release small amounts of pheromone; C. formosanus males cannot follow or reject C. gestroi females as unsuitable. This conclusion was supported by an information-theoretic analysis that detected information flow from C. formosanus females to C. gestroi males as in conspecific pairs, but not from C. gestroi females to C. formosanus males. Despite their following ability, C. gestroi males lost to C. formosanus males in competitions to follow C. formosanus females. Thus, partner selection has shaped the species-specific association of mating pairs. Our results demonstrate that a similar level of coordination can emerge from distinct sets of complementary sender-receiver interactions.

animal behavior and cognition↗

bioRxiv2020

Molecular mapping of qBK1Z, a major QTL for bakanae disease resistance in rice

Bakanae disease is a fungal disease of rice (Oryza sativa L.) caused by the pathogen Gibberella fujikuroi (also known as Fusarium fujikuroi). Recently the disease incidence has increased in several Asian countries and continues to spread throughout the world. No rice varieties have been developed yet to be completely resistant to this disease. With increasing need to identify various genetic resources to impart resistance to local elite varieties, this study was carried out to identify novel quantitative trait loci (QTLs) from an indica variety Zenith. We performed a QTL mapping using 180 F2:9 recombinant inbred lines (RILs) derived from a cross between the resistant variety, Zenith, and the susceptible variety, Ilpum. A primary QTL study using the genotypes and phenotypes of the RILs indicated that the locus qBK1z conferring bakanae disease resistance from the Zenith was located in a 2.8 Mb region bordered by the two SSR markers, RM1331 and RM3530 on chromosome 1. The log of odds (LOD) score of qBK1z was 13.43, accounting for 30.9% of the total phenotypic variation. A finer localization of qBK1z was delimited at an approximate 730 kb interval in the physical map between Chr01_1435908 (1.43 Mbp) and RM10116 (2.16 Mbp). The development of a rice variety with a higher level of resistance against bakanae disease is a major challenge in many rice growing countries. Introducing qBK1z or pyramiding with other previously identified QTLs could provide effective genetic control of bakanae disease in rice.

plant biology↗

bioRxiv2019

M. leprae infects human keratinocytes via the interaction of laminin-5 with α-dystroglycan, integrin-β1, or -β4.

Although Mycobacterium leprae (M. leprae) is usually found in macrophages and nerves of the dermis of patients with multibacillary leprosy, it is also present in all layers of the epidermis, basal, suprabasal, prickle cells, and keratin layers. However, the mechanism by which M.leprae invades the dermis remains unknown, whereas the underlying mechanism by which M.leprae invades peripheral nerves, especially Schwann cells, is well defined. M. leprae binds to the -dystroglycan (DG) of Schwann cells via the interaction of -DG and laminin (LN)-2 in the basal lamina, thus permitting it to become attached to and invade peripheral nerves. In the current study, we investigated the issue of how M.leprae infects keratinocytes. LN-5 is the predominant form of laminin in the epidermis and allows the epidermis to be stably attached to the dermis via its interaction with /{beta}-DG as well as integrins that are produced by keratinocytes. We therefore focused on the role of LN-5 in when M. leprae invades keratinocytes. Our results show that M.leprae preferentially binds to LN-5-coated slides and this binding to LN-5 enhances its binding to human epidermal keratinocytes, neonatal (HEKn). The findings also show that pre-treatment with an antibody against -DG, integrin-{beta}1, or -{beta}4 inhibited the binding of LN-5-coated M.leprae to HEKn cells. These results suggest that M. leprae infects keratinocytes by taking advantage of the interaction of LN-5 in the basal lamina of the epidermis and a surface receptor of keratinocytes, such as -DG, integrin-{beta}1, or -{beta}4.\n\nAuthor summaryIn the current study, we investigated the issue of how M.leprae infects keratinocytes. We focused on the role of LN-5, a predominant form of laminin of the epidermis, in the invasion of M. leprae in keratinocytes. Our results show that M. leprae preferentially binds to LN-5-coated slides and coating M.leprae with LN-5 enhanced its binding to human epidermal keratinocytes, neonatal (HEKn). In addition, a pre-treatment with an antibody against -DG, integrin-{beta}1 or -{beta}4 inhibited the binding of LN-5-coated M. leprae to HEKn cells. These results suggest that M. leprae invades keratinocytes by taking advantage of the interaction of LN-5 in the basal lamina of the epidermis and a surface receptor of keratinocytes, such as -DG, integrin-{beta}1, or -{beta}4

microbiology↗