Community assembly after long-term fragmentation: a case study of tropical rainforest in Xishuangbanna,south-west China

Background: Tropical rainforests represent the most species-rich and at the same time the most fragmented terrestrial biome on Earth. Fragmentation of tropical rainforests is having wide-ranging consequences for the maintenance of local species diversity and community assembly patterns.

Aims: To examine floristic changes and changes in community phylogenetic structure in the forest fragment over the past five decades.

Methods: A new taxonomic diversity algorithm (within-family diversity) was developed to assess floristic changes in the forest fragment. Community phylogenetic structure was then compared before and after fragmentation.

Results: Taxonomic diversity changed greatly among families, with changes occurring randomly across the phylogeny. The forest fragment had higher phylogenetic diversity, higher mean pair-wise phylogenetic distance, but lower mean nearest-neighbour distance. The community phylogenetic structure has changed significantly from clustering to dispersion.

Conclusions: High species turnover occurred in the forest fragment. While shade-tolerant species have been lost, and ruderal and alien species have been added, overall phylogenetic diversity has increased with species being more phylogenetically distant. Competitive exclusion, which was related to the relatively drier conditions in the forest after fragmentation, led the plant community phylogenetic structure to be more dispersed.     

Phylogenies and traits provide distinct insights about the historical and contemporary assembly of aquatic insect communities

The assumption that traits and phylogenies can be used as proxies of species niche has faced criticisms. Evidence suggested that phylogenic relatedness is a weak proxy of trait similarity. Moreover, different processes can select different traits, giving opposing signals in null model analyses. To circumvent these criticisms, we separated traits of stream insects based on the concept of α and β niches, which should give clues about assembling pressures expected to act independently of each other. We investigated the congruence between the phylogenetic structure and trait structure of communities using all available traits and all possible combinations of traits (4095 combinations). To account for hierarchical assembling processes, we analyzed patterns on two spatial scales with three pools of genera. Beta niche traits selected a priori – i.e., traits related to environmental variation (e.g., respiration type) – were consistently clustered on the smaller scale, suggesting environmental filtering, while α niche traits – i.e., traits related to resource use (e.g., trophic position) – did not display the expected overdispersion, suggesting a weak role of competition. Using all traits together provided random patterns and the analysis of all possible combinations of traits provided scenarios ranging from strong clustering to overdispersion. Communities were phylogenetically overdispersed, a pattern previously interpreted as phylogenetic limiting similarity. However, our results likely reflect the co‐occurrence of ancient clades due to the stability of stream habitats along the evolutionary scale. We advise ecologists to avoid using combinations of all available traits but rather carefully traits based on the objective under consideration. Both trait and phylogenetic approaches should be kept in the ecologist toolbox, but phylogenetic distances should not be used as proxies of traits differences. Although the phylogenetic structure revealed processes operating at the evolutionary scale, only specific traits explained local processes operating in our communities.     

CCDC115 Deficiency Causes a Disorder of Golgi Homeostasis with Abnormal Protein Glycosylation

Disorders of Golgi homeostasis form an emerging group of genetic defects. The highly heterogeneous clinical spectrum is not explained by our current understanding of the underlying cell-biological processes in the Golgi. Therefore, uncovering genetic defects and annotating gene function are challenging. Exome sequencing in a family with three siblings affected by abnormal Golgi glycosylation revealed a homozygous missense mutation, c.92T>C (p.Leu31Ser), in coiled-coil domain containing 115 (CCDC115), the function of which is unknown. The same mutation was identified in three unrelated families, and in one family it was compound heterozygous in combination with a heterozygous deletion of CCDC115. An additional homozygous missense mutation, c.31G>T (p.Asp11Tyr), was found in a family with two affected siblings. All individuals displayed a storage-disease-like phenotype involving hepatosplenomegaly, which regressed with age, highly elevated bone-derived alkaline phosphatase, elevated aminotransferases, and elevated cholesterol, in combination with abnormal copper metabolism and neurological symptoms. Two individuals died of liver failure, and one individual was successfully treated by liver transplantation. Abnormal N- and mucin type O-glycosylation was found on serum proteins, and reduced metabolic labeling of sialic acids was found in fibroblasts, which was restored after complementation with wild-type CCDC115. PSI-BLAST homology detection revealed reciprocal homology with Vma22p, the yeast V-ATPase assembly factor located in the endoplasmic reticulum (ER). Human CCDC115 mainly localized to the ERGIC and to COPI vesicles, but not to the ER. These data, in combination with the phenotypic spectrum, which is distinct from that associated with defects in V-ATPase core subunits, suggest a more general role for CCDC115 in Golgi trafficking. Our study reveals CCDC115 deficiency as a disorder of Golgi homeostasis that can be readily identified via screening for abnormal glycosylation in plasma.     

Organoids and the genetically encoded self‐assembly of embryonic stem cells

Understanding the mechanisms of early embryonic patterning and the timely allocation of specific cells to embryonic regions and fates as well as their development into tissues and organs, is a fundamental problem in Developmental Biology. The classical explanation for this process had been built around the notion of positional information. Accordingly the programmed appearance of sources of Morphogens at localized positions within a field of cells directs their differentiation. Recently, the development of organs and tissues from unpatterned and initially identical stem cells (adult and embryonic) has challenged the need for positional information and even the integrity of the embryo, for pattern formation. Here we review the emerging area of organoid biology from the perspective of Developmental Biology. We argue that the events underlying the development of these systems are not purely linked to “self‐organization,” as often suggested, but rather to a process of genetically encoded self‐assembly where genetic programs encode and control the emergence of biological structures.     

Local contagion and regional compression: habitat selection drives spatially explicit,multiscale dynamics of colonisation in experimental metacommunities

Habitat selection, including oviposition site choice, is an important driver of community assembly in freshwater systems. Factors determining patch quality are assessed by many colonising organisms and affect colonisation rates, spatial distribution and community structure. For many species, the presence/absence of predators is the most important factor affecting female oviposition decisions. However, individual habitat patches exist in complex landscapes linked by processes of dispersal and colonisation, and spatial distribution of factors such as predators has potential effects beyond individual patches. Perceived patch quality and resulting colonisation rates depend both on risk conditions within a given patch and on spatial context. Here we experimentally confirm the role of one context‐dependent processes, spatial contagion, functioning at the local scale, and provide the first example of another context‐dependent process, habitat compression, functioning at the regional scale. Both processes affect colonisation rates and patterns of spatial distribution in naturally colonised experimental metacommunities.     

Introductions do not compensate for functional and phylogenetic losses following extinctions in insular bird assemblages

The ratio of species extinctions to introductions has been comparable for many insular assemblages, suggesting that introductions could have ‘compensated’ for extinctions. However, the capacity for introduced species to replace ecological roles and evolutionary history lost following extinction is unclear. We investigated changes in bird functional and phylogenetic diversity in the wake of extinctions and introductions across a sample of 32 islands worldwide. We found that extinct and introduced species have comparable functional and phylogenetic alpha diversity. However, this was distributed at different positions in functional space and in the phylogeny, indicating a ‘false compensation’. Introduced and extinct species did not have equivalent functional roles nor belong to similar lineages. This makes it unlikely that novel island biotas composed of introduced taxa will be able to maintain ecological roles and represent the evolutionary histories of pre‐disturbance assemblages and highlights the importance of evaluating changes in alpha and beta diversity concurrently.     

The hairpin region of Ndc80 is important for the kinetochore recruitment of Mph1/MPS1 in fission yeast

The establishment of proper kinetochore-microtubule attachments facilitates faithful chromosome segregation. Incorrect attachments activate the spindle assembly checkpoint (SAC), which blocks anaphase onset via recruitment of a cohort of SAC components (Mph1/MPS1, Mad1, Mad2, Mad3/BubR1, Bub1 and Bub3) to kinetochores. KNL1, a component of the outer kinetochore KMN network (KNL1/Mis12 complex/Ndc80 complex), acts as a platform for Bub1 and Bub3 localization upon its phosphorylation by Mph1/MPS1. The Ndc80 protein, a major microtubule-binding site, is critical for MPS1 localization to the kinetochores in mammalian cells. Here we characterized the newly isolated mutant ndc80-AK01 in fission yeast, which contains a single point mutation within the hairpin region. This hairpin connects the preceding calponin-homology domain with the coiled-coil region. ndc80-AK01 was hypersensitive to microtubule depolymerizing reagents with no apparent growth defects without drugs. Subsequent analyses indicated that ndc80-AK01 is defective in SAC signaling, as mutant cells proceeded into lethal cell division in the absence of microtubules. Under mitotic arrest conditions, all SAC components (Ark1/Aurora B, Mph1, Bub1, Bub3, Mad3, Mad2 and Mad1) did not localize to the kinetochore. Further genetic analyses indicated that the Ndc80 hairpin region might act as a platform for the kinetochore recruitment of Mph1, which is one of the most upstream SAC components in the hierarchy. Intriguingly, artificial tethering of Mph1 to the kinetochore fully restored checkpoint signaling in ndc80-AK01 cells, further substantiating the notion that Ndc80 is a kinetochore platform for Mph1. The hairpin region of Ndc80, therefore, plays a critical role in kinetochore recruitment of Mph1.