Search

Around the world, land-use change caused by human-activity threatens biodiversity, which often results in forest loss and fragmentation, and the loss of forest biodiversity. Forest loss and fragmentation resulting from plantations can have a substantial impact on bird communities because plantations are essentially less suitable environments for bird communities than natural forests. Woodpeckers inhabiting large trees are particularly susceptible to forest loss and fragmentation. They play a critical role in the ecosystem, as they not only create tree cavities, but might also contribute to the number of tree falls. Their functions are indispensable and cannot be substituted by those of other species. A decline in woodpecker numbers due to forest loss and fragmentation is likely to change forest ecosystems in various ways. This study examined whether the fragmentation and loss of natural forests has resulted in a decline in the woodpecker population, resulting in reduced number of tree cavities, and consequently, a reduced number of tree falls. The results of this study indicate that the number of fallen trees was positively related to the number of woodpeckers through the number of tree cavities they created. In addition, forest loss, not forest fragmentation, was related to decrease in woodpecker abundance, leading to negative cascading effects on the number of tree cavities and fallen trees. Forest loss changed the woodpecker community structure by affecting the woodpecker guilds differently. Conserving large broad-leaved forests could contribute to the conservation of specific woodpecker species and their roles in the ecosystem.

The transcription factor NFATc1 and its binding partner AP-1 (a complex containing c-fos and c-Jun) play a central role in osteoclast differentiation. NFATc1 and AP-1 promote the expression of target genes such as Acp5, Ctsk and also auto-regulate NFATc1 expression as well. We previously reported that protein phosphatase 1 regulatory subunit 18 (PPP1r18) is a negative regulator of osteoclast bone resorption by inhibiting cell attachment to bone matrix. We also reported that PPP1r18 potentially regulates NFATc1 expression during osteoclast differentiation. To further explore this, in this study we have examined the effect of PPP1r18 on NFATc1 expression and activity by overexpressing PPP1r18 during the early stage of osteoclast differentiation. We found that PPP1r18 suppressed NFATc1 expression through inhibition of the transcriptional activity of NFATc1. Since PPP1r18 does not regulate NFATc1 directly, we next explored the involvement of AP-1. Our data showed that c-fos phosphorylation and nuclear localization were reduced by PPP1r18 overexpression. Further experiments showed that overexpression of c-fos together with PPP1r18 rescued NFATc1 expression and transcriptional activity. Moreover, c-fos activity inhibition by PPP1r18 was canceled by mutation of the phosphatase binding site of PPP1r18. Taken together, PPP1r18-regulated phosphatase activity targets c-fos phosphorylation and suppresses subsequent NFATc1 expression and activity.