## 1 Introduction  
Myo/Nog (M/N) cells were first identified in the chick embryo blastocyst, where they express MyoD, a muscle-specific transcription factor; Noggin, a bone morphogenetic protein (BMP) inhibitor; and brain-specific angiogenesis inhibitor 1 (BAII) [1, 2]. Their critical functions in early development have been demonstrated, with studies showing that the absence of Myo/Nog cells results in severe malformations, including the lack of skeletal muscle formation, central nervous system defects, and various ocular abnormalities such as anophthalmia, lens dysgenesis, and retinal overgrowth [3].  
Beyond embryonic development, Myo/Nog cells persist in multiple tissues of adult organisms, including mice, rats, rabbits, and humans. Previous research has exploredtheir role in ocular and systemic pathologies, demonstrating their capacity to respond to tissue injury. In the lens, these cells localize to wound sites, differentiate into contractile myofibroblasts, and contribute to posterior capsule opacification, a common complication following cataract surgery [4]. Their depletion in murine models of retinopathy of prematurity results in increased neuronal apoptosis, while their addition to the vitreous cavity following light-induced retinal damage enhances cell survival and preserves visual function [5]. Additionally, neuroprotective properties of Myo/Nog cells have been documented in models of ocular hypertension and localized brain injuries [6; 7].  
Although Myo/Nog cells respond to injury in the eye, the mechanisms through which they mediate neuroprotection are unknown. Most prior studies have focused on acute and artificially induced models of ocular pathology, limiting our understanding of Myo/Nog cell behavior in chronic retinal conditions. The role and anatomical locations of the Myo/Nog cells in a naturally occurring model of ocular pathology have not been looked at before. This study differs from prior research that focused on acute injury models by utilizing a congenital retinitis pigmentosa model, allowing us to examine Myo/Nog cell behavior during natural disease progression. For this, we used the C3H/HeJ mouse strain, which is homozygous for the cGMP phosphodiesterase 6B (PDE6) mutation, also known as the rd1 mutation. PDE6 is in the outer segments of photoreceptors and is an essential part of the visual signaling cascade [8]. In mice with the PDE6 mutation, an accumulation of intracellular cGMP leads to the deleterious influx of Ca2+ into the cell, which consequently leads to rod cell death through a mechanism likely mediated by apoptosis-inducing factor (AIF) in the mitochondria [9; 10; 11]. Rod cell death begins at postnatal day 7 (P7) and progresses quickly for 3-4 weeks [12]. Mice retain some pattern recognition ability up to postnatal day 40 (P40). Like humans with RP, the mutation eventually affects cones and leads to complete blindness by 6 weeks of age [13]. Other widely used models of RP include the rd10 mouse, which exhibits slower degeneration, and the Rho\({}^{-}\)/\({}^{-}\) mouse, which lacks rhodopsin and undergoes rapid rod degeneration. Compared to these models, the C3H/HeJ strain offers a consistent, faster, and well-characterized timeline of degeneration useful for studying early to late-stage retinal pathology within a month after birth.  
This study aims to quantify Myo/Nog cell distribution in response to retinal degeneration and assess their phagocytic activity in the ONL based on BAII's known function as a mediator of phagocytosis [14] and our previous study in which Myo/Nog cells internalized tattoo ink, dead cells in lens cultures, and microbeads injected into the anterior chamber of the eye [15].