Metacommunity dynamics and the detection of species associations in co-occurrence analyses: why patch disturbance matters

Abstract

Many methods attempt to detect species associations from co-occurrence patterns. Such associations are then typically used to infer inter-specific interactions. However, correlation is not equivalent to interaction. Habitat heterogeneity and out-of-equilibrium colonization histories are acknowledged to cause species associations even when inter-specific interactions are absent. Here we show how classical metacommunity dynamics, within a homogeneous habitat at equilibrium, can also lead to statistical associations. This occurs even when species do not interact. All that is required is patch disturbance (i.e. simultaneous extinction of several species in a patch) a common phenomenon in a wide range of real systems. We compare direct tests of pairwise independence, matrix permutation approaches and joint species distribution modelling. We use mathematical analysis and example simulations to show that patch disturbance leads all these methods to produce characteristic signatures of spurious association from "null" co-occurrence matrices. Including patch age (i.e. the time since the last patch disturbance event) as a covariate is necessary to resolve this artefact. However, this would require data that very often are not available in practice for these types of analyses. We contend that patch disturbance is a key (but hitherto overlooked) factor which must be accounted for when analysing species co-occurrence.

Clonal hematopoiesis driven by DNMT3A and TET2 mutations: role in monocyte and macrophage biology and atherosclerotic cardiovascular disease

“…Tet2 deficiency in murine macrophages results in inflammasome activation and an enhanced secretion of IL-1B and IL-6 [26,46]. Moreover, activation of type I interferons by Interferon Response Factor 3 (IRF3), known to promote an adverse response to MI [56], is regulated by NLRP3, TET2 and nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2) (Calcagno et al, 2020, BioRxive) [57]. The distinctions between Tet2 deficient BMDM and PM support context-specific roles of TET2 in macrophages, similar to observations with DNMT3A.…”