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Agha, M.

Publications and source records attributed to Agha, M..

3 recordsLinked to original sources

Conservation genomics of desert tortoises (Gopherus agassizii) in the Colorado Desert

Management units (MUs) are important to conserving species of conservation concern. Although the MU definition is simple (i.e., a demographically independent population), identifying MUs in practice is difficult because investigators must choose a recent (i.e., last few generations) migration rate threshold. One suggested MU criterion is m < 0.10, where m is the proportion of a subpopulation comprised of recent migrants. However, a more recent study found that m as low as 0.02 (i.e., one migrant per generation) can cause estimates of linkage disequilibrium effective population size (NeLD) to underestimate a subpopulations true Ne. Here, we used genome-wide SNP data obtained from 40 tortoises and an MU criterion of m < 0.02 to define MUs within the Colorado Desert population of the Mojave desert tortoise (Gopherus agassizii)--an endangered species in California and a species in the USA protected under the Endangered Species Act. Based on our results we defined the Mesa and Deep Canyon subpopulations as MUs even though the latter received at least two recent immigrants. Migrant(s) from the Shavers Valley subpopulation were likely translocated by humans, whereas migrant(s) from the Mesa subpopulation could have been human-mediated or natural migrants. Initial analyses suggest that the Shavers Valley subpopulation may be an MU, but our low sample size renders this result inconclusive. The local Ne estimates for the Mesa and Deep Canyon subpopulations--5 and 13 adults, respectively--are below the minimum sizes according to the 50/500 rule and thus they may be candidates for genetic rescue.

genomics↗

Defense-Suppressive Fragments of RIN4 generated by AvrRpt2 Participate in NDR1-dependent Activation of RPS2

Plant nucleotide-binding, leucine-rich-repeat (NLR) immune receptors recognize pathogen effectors and activate immunity. The NLR RPS2 recognizes AvrRpt2, a Pseudomonas effector that promotes virulence by proteolytically cleaving a membrane-tethered host protein, RIN4. RIN4 cleavage by AvrRpt2 generates fragments that activate RPS2. A model for RPS2 activation by RIN4 destruction is consistent with the ectopic activity of RPS2 in plants lacking RIN4 but does not explain the link between AvrRpt2s virulence activity and RPS2 activation. We found that non-membrane-tethered RIN4 derivatives are potent cytosolic activators of RPS2. Activation of RPS2 by these RIN4 derivatives, like AvrRpt2-induced activation, and unlike ectopic activation in the absence of RIN4, requires the defense signaling protein NDR1. Cleavage products of RIN4 produced by AvrRpt2 play contrasting roles in the activation of RPS2, with the membrane-tethered C-terminal fragment suppressing RPS2 and the non-membrane-tethered internal fragment, dependent on compatibility with the C-terminal fragment, overcoming its suppression of RPS2. HighlightsO_LINon-membrane tethered derivatives of RIN4 activate RPS2-induced cell death C_LIO_LIActivation of RPS2 by non-membrane-tethered derivatives of RIN4 requires NDR1 C_LIO_LIAvrRpt2-induced cleavage fragments of RIN4 play contrasting roles in RPS2 activation C_LI

plant biology↗

Cell-type-specific origins of spinal rhythmicity at different locomotor speeds in larval zebrafish

Different speeds of locomotion require heterogeneous spinal populations, but a common mode of rhythm generation is presumed to exist. Here, we explore the cellular versus synaptic origins of spinal rhythmicity at different speeds by performing electrophysiological recordings from premotor excitatory interneurons in larval zebrafish. Chx10-labeled V2a neurons are divided into at least two morphological subtypes proposed to play distinct roles in timing and intensity control. Consistent with distinct rhythm generating and output patterning functions within the spinal V2a population, we find that descending subtypes are recruited exclusively at slow or fast speeds and exhibit intrinsic cellular properties suitable for rhythmogenesis at those speeds, while bifurcating subtypes are recruited more reliably at all speeds and lack appropriate rhythmogenic cellular properties. Unexpectedly, however, phasic firing patterns during locomotion in rhythmogenic and non-rhythmogenic V2a neurons alike are best explained by distinct modes of synaptic inhibition linked to cell-type and speed. At fast speeds reciprocal inhibition in descending V2a neurons supports phasic firing, while recurrent inhibition in bifurcating V2a neurons helps pattern motor output. In contrast, at slow speeds recurrent inhibition in descending V2a neurons supports phasic firing, while bifurcating V2a neurons rely on reciprocal inhibition alone to pattern output. Our findings suggest cell-type-specific, not common, modes of rhythmogenesis generate and coordinate different speeds of locomotion.

neuroscience↗